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The dormant blood microbiome in chronic, inflammatory diseases

Marnie Potgieter, Janette Bester, Douglas B. Kell and 1 more

FEMS Microbiology Reviews · 2015 · Review

doi:10.1093/femsre/fuv013

Abstract

Blood in healthy organisms is seen as a 'sterile' environment: it lacks proliferating microbes. Dormant or not-immediately-culturable forms are not absent, however, as intracellular dormancy is well established. We highlight here that a great many pathogens can survive in blood and inside erythrocytes. 'Non-culturability', reflected by discrepancies between plate counts and total counts, is commonplace in environmental microbiology. It is overcome by improved culturing methods, and we asked how common this would be in blood. A number of recent, sequence-based and ultramicroscopic studies have uncovered an authentic blood microbiome in a number of non-communicable diseases. The chief origin of these microbes is the gut microbiome (especially when it shifts composition to a pathogenic state, known as 'dysbiosis'). Another source is microbes translocated from the oral cavity. 'Dysbiosis' is also used to describe translocation of cells into blood or other tissues. To avoid ambiguity, we here use the term 'atopobiosis' for microbes that appear in places other than their normal location. Atopobiosis may contribute to the dynamics of a variety of inflammatory diseases. Overall, it seems that many more chronic, non-communicable, inflammatory diseases may have a microbial component than are presently considered, and may be treatable using bactericidal antibiotics or vaccines.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 17, 2026. Paragraph numbers are ours, so an answer can point at one.

INTRODUCTION

‘Overall, it seems inevitable that the availability of these methods will cause the catalog of disease states recognized as having a microbial contribution to their etiology to expand enormously in the short term, particularly as improved methods for resuscitation of small cell numbers are found’ (Davey and Kell ).

Over the years, a variety of diseases that were previously considered non-communicable have been found to have a microbial component, the role of Helicobacter pylori in ulcerogenesis (Marshall and Warren ) being a particularly well-known example. There have also been hints for a microbial component to many other non-communicable diseases, but culturing the relevant organisms has rarely been successful. However, there is increasing recognition that microbes may be present in forms that are not easily culturable, and a number of recent articles have brought these possibilities more sharply into focus. Our aim is to review these developments. The manuscript structure is shown in Fig. 1.

A note on terminology: viable, culturable, dormant and sterile

In this field, much confusion has arisen historically because of a failure to recognize that most microbes reproduce by binary fission and that this reproduction must be a minimal property or hallmark of a microbial cell that possesses ‘life’ or is ‘alive’ (Proal, Albert and Marshall ). Thus, as with Schrödinger's cat (e.g. Primas; Gribbin ), we cannot say that an individual microbial cell ‘is’ alive, only (if true) that it ‘was’ alive, since it will by then have become two cells. This implies that being alive is not best treated as though it were an innate property of a cell, but the definition must be operational, and include both the cell and the ‘environment’ (experiment) used to detect the status a posteriori (Kell et al. ).

Thus, as with Postgate (e.g. Postgate,, ), we equate viability with culturability, and stress that culturability—the ability to reproduce—is to be determined operationally. Other methods that do not determine culturability are not tests of viability per se, but merely measure what they measure (e.g. the content of a chemical such as ATP, membrane permeability to a dye, enzymatic activity, macromolecular sequences and so on). In addition, it is impossible in principle to (cor)relate macroscopic measurements of a culture with the ability of individual cells to divide (Kell et al.; Davey and Kell ). In other words, if the macroscopic ATP content of say a starving culture were to decrease by 50%, we would not know if all of the cells had lost half their ATP or half of the cells had lost all of their ATP (or anything in between). The culturability of the former would likely be 50% and of the latter 100%, despite the same macroscopic ATP content.

A lack of culturability may mean that a cell is non-viable under the circumstances tested, but viability or non-viability are not the only two possible states here. An apparent non-culturability of a surviving cell also admits another possibility, for which the natural term is ‘dormant’ (Kaprelyants, Gottschal and Kell; Epstein ). This is that the cell is not presently culturable (viable), but it is not ‘dead’ (in the sense of an operationally irreversible loss of viability) in that it may be induced to return to a state of culturability (by a process or processes typically referred to as ‘resuscitation’). This also means that the term ‘viable-but-non-culturable’, while quite common in use, is in fact an oxymoron that is to be discouraged (Kell et al. ). The eminent microbial physiologist Howard Gest is similarly scathing about the term ‘unculturable’ (Gest ), noting that one just needs to try harder to culture organisms. Table 1 shows the three terms best suited to discuss these issues, while Fig. 2 shows a diagrammatic representation of the macroscopic physiological microbial states we mostly consider.

The assessment of replication potential (culturability) of individual cells may be done microscopically (e.g. by microscopic counts) or macroscopically (e.g. via colony formation on an agar plate or through the ‘most probable number’ technique). The latter has the advantage of potentially assessing dormancy in the absence of any contaminating culturable cells that might proliferate during the assay (Kaprelyants, Mukamolova and Kell; Votyakova, Kaprelyants and Kell; Kell et al. ). For assessing culturability (=viability), we do not therefore include other strategies in which cells do not actually divide, such as the so-called direct viable count of Kogure, Simidu and Taga. Thus, we here highlight the point that the possibility of microbial dormancy means that a system that appears to be devoid of culturable microbes may still contain dormant cells or forms that may become culturable.

The ‘sterile’ blood microbiome brought into question

The circulation is a closed system and the blood in healthy organisms was first believed to be a sterile environment (Drennan; Proal, Albert and Marshall ). This definition is used in the most usual sense of an absence of culturable microbes, since blood can of course provide a suitable growth medium for microbes (as in blood culture; Wilson and Weinstein; Weinstein; Schroeter et al.; cf. Valencia-Shelton and Loeffelholz ), and any bacteraemia or sepsis, even at 1–10 cells mL−1 (Murray ), is potentially life-threatening (e.g. Vincent et al.; Eleftheriadis et al.; Havey, Fowler and Daneman; Montassier et al. ). However, the principle of the presence of truly sterile blood in healthy humans has been challenged, as operationally it does not mean that dormant or non-culturable forms of organisms are absent (Kaprelyants, Gottschal and Kell; Kell et al.; McLaughlin et al. ) (see Table 1). Nearly 50 years ago, the existence of a novel bacteriological system was noted in 71% of blood samples taken from diseased humans and from 7% of supposedly healthy humans, when RBCs were lysed (Domingue and Schlegel ). A year later, corynebacteria-like microorganisms developing in hemocultures were shown within RBCs (Tedeschi et al. ), and in 2001 it was found that even ‘healthy’ blood specimens can contain bacterial 16S ribosomal DNA (Nikkari et al. ). Domingue and Woody and Domingue summarizes much of this earlier literature. L-forms are bacterial variants that lack some or all of a cell wall. Nonetheless they can divide, especially in osmotically stabilized media, by processes that variously involve membrane blebbing, tubulation, vesiculation and fission (Allan, Hoischen and Gumpert; Errington; Mercier, Kawai and Errington ). While it remains unclear whether what was seen in these earlier studies (Domingue and Woody; Domingue ) may have been L-forms (Mattman ), that could in time revert to normal bacteria under the correct conditions (Casadesús ), L-forms are becoming a topic of considerable current research (Devine; Domínguez-Cuevas et al.; Mercier, Kawai and Errington, ).

The presence of a blood bacterial microbiome has also been associated with a variety of infectious, as well as non-infectious disease states (Huang et al.; Thwaites and Gant; Nielsen et al.; Prajsnar et al.; Wang et al.; Kibru et al.; Sato et al. ). It is, for example, known that H. pylori can exist not only in the gastric mucosa but also in peripheral blood, where it could cause bacteremia (Huang et al. ), and could contribute to Parkinson's disease (PD) or related pathologies that precede motor symptoms (Nielsen et al. ). Helicobacter pylori was also previously implicated in the development of anemia (Wang et al.; Kibru et al. ). Staphylococcus aureus can also use neutrophils as ‘Trojan horses’ to disseminate infection (Thwaites and Gant; Prajsnar et al. ), while many other pathogens, such as Listeria monocytogenes (Xayarath and Freitag ), Salmonella typhimurium (Eisenreich et al.; Claudi et al.; Holden ) and Yersinia pestis (Isberg ), are well known to persist intracellularly; Gest gives other historical examples. The same is true for viruses, which are not discussed here.

The presence of an aberrant blood microbiota (as assessed by sequencing) has been implicated in type II diabetes and cardiovascular disease (Amar et al.,; Sato et al. ). There is also growing evidence that periodontal disease and gingivitis are closely linked to cardiovascular disease (Yang et al.; Ramírez et al. ). Oral bacterial translocation into the blood has been implicated in the development of periodontal disease-induced endocarditis and myocardial and/or cerebral infarction, especially in patients with heart valve dysfunction (Koren et al.; Amar and Engelke; Seringec et al. ).

We will argue in the next sections that the existence of potentially viable (but possibly non-proliferating) pleomorphic bacteria in the blood of healthy humans (McLaughlin et al. ) may therefore be of some significance in pathology. If such a microbiome can disrupt homeostasis, it can ultimately play a fundamental role in disease development and progression. It has therefore been proposed that the blood microbiota might therefore represent or contribute to the first step in the kinetics of atherosclerosis (Sato et al. ), cardiovascular disease and type II diabetes (Amar et al. ), and therefore ultimately serve as biomarkers for cardiovascular disease risk (Amar et al. ). However, in the quest to use the blood microbiota as biomarkers, the question of detectability and cultivability are key concepts.

In particular, the existence of a blood microbiome is only really meaningful and of scientific interest if it represents an undisturbed state, and is not, for instance, an artefact caused by the external introduction of microbes through human intervention, reagent contamination (Schroeter et al.; Salter et al. ) and so forth. We therefore rehearse the evidence that while such artefacts are certainly possible, and must be excluded rigorously, the phenomenon of a human blood microbiome cannot be dismissed as such an artefact in toto.

Evidence that these observations are not due to contamination

While contamination from reagents (e.g. Schroeter et al.; Salter et al. ), or simply poor sterile technique with needles and so on, can lead to an artefactual appearance of a blood microbiome, we consider that the following arguments, taken together, exclude the thought that the entire (and considerable) literature on a blood microbiome can be explained via contamination. The first argument is that there are significant differences between the blood microbiomes of individuals harboring disease states and nominally healthy controls, despite the fact that samples are treated identically (see later). Some similar arguments apply to the assessment of drug transporters under different conditions (Kell and Oliver ).A second argument is that the morphological type of organism (e.g. coccus versus bacillus) seems to be characteristic of particular diseases.A third argument is that in many cases (see below) relevant organisms lurk intracellularly, which is hard to explain by contamination.A fourth argument is that there are just too many diseases where bacteria have been found to play a role in the pathogenesis, that all of them may be caused by contamination.Finally, the actual numbers of cells involved seem far too great to be explicable by contamination; given that blood contains more than 109 erythrocytes mL−1, if there was just one bacterial cell per 100 000 erythrocytes (see below and Amar et al. ), this will equate to 104 bacteria mL−1. These are not small numbers.

The first argument is that there are significant differences between the blood microbiomes of individuals harboring disease states and nominally healthy controls, despite the fact that samples are treated identically (see later). Some similar arguments apply to the assessment of drug transporters under different conditions (Kell and Oliver ).

A second argument is that the morphological type of organism (e.g. coccus versus bacillus) seems to be characteristic of particular diseases.

A third argument is that in many cases (see below) relevant organisms lurk intracellularly, which is hard to explain by contamination.

A fourth argument is that there are just too many diseases where bacteria have been found to play a role in the pathogenesis, that all of them may be caused by contamination.

Finally, the actual numbers of cells involved seem far too great to be explicable by contamination; given that blood contains more than 109 erythrocytes mL−1, if there was just one bacterial cell per 100 000 erythrocytes (see below and Amar et al. ), this will equate to 104 bacteria mL−1. These are not small numbers.

It is important to point out that molecular methods have been used frequently to detect active sepsis. These selfsame methods are also used in environmental biology (as we pointed out in this review), without undue concern about the potential for contamination. Contamination will always be a concern, of course, as noted by Nikkari et al., but many papers since 2001 have documented strategies for detecting prokaryotic DNA in blood and serum using appropriate and careful controls (Anthony et al.; Mylotte and Tayara; Jiang et al.; Varani et al.; Mancini et al.; Chang et al.; Grif et al.; Fernández-Cruz et al.; Gaibani et al. ). Also, detecting bacteria in blood cultures during sepsis is considered the standard diagnostic tool for blood stream infections (Muñoz et al.; Varani et al. ), and some laboratories consider that e.g. PCR testing should always be a complement for the traditional blood culture test (Grif et al. ).

The role of dormancy

Dormancy in microbiology is of course well known, even for non-sporulating bacteria, and has been defined as a stable but reversible nonreplicating state (Mariotti et al.; see also Table 1 and Kaprelyants, Gottschal and Kell; Kell et al., ). The importance of dormant or non-cultured (as opposed to ‘non-culturable’) organisms has long been recognized in environmental microbiology (e.g. Mason, Hamer and Bryers; Amann, Ludwig and Schleifer; Eilers et al.; Hugenholtz; Keller and Zengler; Pham and Kim; Epstein ), because of the 100-fold or greater difference between microscopically observable cells and those capable of forming a colony on an agar plate (‘the great plate count anomaly’, see below).

Of the four main possibilities, what we do not know in general is whether the ‘missing’ cells are incapable of growth on the enrichment/isolation media,are killed by the enrichment/isolation media (e.g. Tanaka et al. ),have lost viability irreversibly (i.e. are operationally dead) orare in a dormant or not-immediately-culturable state from which we might resuscitate them (to effect culturability) if only we knew how.

are incapable of growth on the enrichment/isolation media,

are killed by the enrichment/isolation media (e.g. Tanaka et al. ),

have lost viability irreversibly (i.e. are operationally dead) or

are in a dormant or not-immediately-culturable state from which we might resuscitate them (to effect culturability) if only we knew how.

The fact that typical isolation media and incubation conditions do not admit the measurable growth of all strains is certainly well known (indeed it is the basis for selective isolation media!), and it took a good while to learn how to culture pathogens such as H. pylori (Marshall and Warren; Marshall ), Legionella pneumophila (Feeley et al.; Saito et al.; Meyer ), Tropheryma whipplei (Maiwald and Relman; Maiwald et al.; Renesto et al. ) and so on (Singh et al. ). The majority of bacteria that persist in a ‘non-culturable’ form in wounds (e.g. Dowd et al.; Percival et al. ), or in diseases such as cystic fibrosis (Lewis ) or tuberculosis (Young, Stark and Kirschner; Zhang, Yew and Barer ), and even simply in conventional cultures of Escherichia coli (e.g. Koch; Balaban et al.; Keren et al.,; Gerdes and Maisonneuve; Amato, Orman and Brynildsen; Germain et al.; Maisonneuve, Castro-Camargo and Gerdes; Maisonneuve and Gerdes; Holden ), where phenotypic culture differentiation is well established (Koch ), are also ‘normally culturable’ by established means. Thus, the existence of operationally ‘non-culturable’ forms of only moderately fastidious bacteria is very well established, and more and more bacteria previously thought ‘unculturable’ are being brought into culture (e.g. Zengler et al.; Keller and Zengler; Stevenson et al.; Gich et al.; Kamagata and Tamaki; D'Onofrio et al.; Nichols et al.; Vartoukian, Palmer and Wade; Dedysh; Pham and Kim; Puspita et al.,; Stewart; Allen-Vercoe; Narihiro and Kamagata; Singh et al.; Walker et al.; Lagier et al.,; Ling et al. ).

In environmental microbiology, some bacteria pass through the usual 0.2 μm filters, and have been referred to as ‘ultramicrobacteria’ (Macdonell and Hood; Morita ). It was proposed (Kaprelyants, Gottschal and Kell ) that rather than being small (starved) forms of normal bacteria they were more likely to be normal forms of small bacteria, and this seems to have been accepted (Lysak et al.; Sahin et al.; Duda et al.; Soina et al. ).

The ability to culture certain kinds of soil bacteria by preincubation in weak broth is also well established (e.g. Bakken and Olsen; Kaprelyants, Gottschal and Kell ), and our own experiments showed very high levels of resuscitability of dormant cells of Micrococcus luteus (e.g. Kaprelyants and Kell; Kaprelyants, Mukamolova and Kell; Kaprelyants et al.,; Kell et al.,; Mukamolova et al.,,,,). In a similar way, substrate-accelerated death of non- or slowly growing microorganisms has been known for decades (Postgate; Calcott and Postgate; Calcott and Calvert ).

Thus, any of several well-established mechanisms may contribute to the (often) large differences observable between microscopic counts and the number of operationally culturable microbes, with the greatest likelihood being that we simply have to develop more and better methods to bring these strains back into culture, i.e. to resuscitate them. In particular, however, this ‘great plate count anomaly’ has, of course, been brought into much sharper focus because of the advent of culture-independent, sequence-based means for detecting and (to a certain extent) enumerating microbes (though not, of course, of assessing their culturability).

Sequence-based methods for detecting non-proliferating microbes

The vast majority of microbial species remain uncultivated and, until recently, about half of all known bacterial phyla were identified only from their 16S ribosomal RNA gene sequence (Lasken and McLean ). Also, single-cell genomics is a powerful tool for accessing genetic information from uncultivated microorganisms (Lasken; Rinke et al.; Cavanagh et al.; Clingenpeel et al. ). Bacterial single-cell genome sequencing and bioinformatics are, however, challenging (Pallen, Loman and Penn; Didelot et al.; Loman et al.; Fricke and Rasko ).

The development of sequence-based methods for microbes (and especially non-eukaryotes) owes much to the pioneering work of Carl Woese and colleagues, who recognized the utility of small subunit ribosomal RNA (based on both its essentiality and the small but significant sequence variations) and applied it with great effect in molecular phylogenetics (Woese and Fox; Woese, Kandler and Wheelis ). Notwithstanding modern reinterpretations of the taxonomic details derived therefrom (e.g. Williams et al. ), there can be little doubt that this work drew the attention of microbiologists to the potential of sequence-based methods for detecting microbes that were then invisible to methods based solely on culture, e.g. in clinical microbiology (Didelot et al.; Loman et al.; Proal et al.; Fricke and Rasko ). rRNA remains a widely used strategy for detecting specific microbes. This has of course led to metagenomics, the large-scale sequencing of macromolecules and indeed (statistically) entire genomes from complex (non-axenic) environments, increasing the requirement for a full set of complete reference sequences (Kyrpides et al. ) and not just those of 16S rRNA (Yarza et al. ). Even the coupling of sequences to activities has now become possible (e.g. Radajewski et al.; Wang et al. ).

Microbiome analyses: latest technologies employed

More recently, gut metagenomics has been systematized with NIH's Human Microbiome project (HMP) and the European MetaHIT project aiming to deciphering the structure and function of the human gut microbiota (Fredricks; Robles-Alonso and Guarner ). The HMP has developed a reference collection of 16S ribosomal RNA gene sequences collected from sites across the human body (Koren et al.; Ding and Schloss ). This information can be used to associate changes in the microbiome with changes in health, and particularly also the blood microbiome. The Integrative Human Microbiome Project (iHMP, http://hmp2.org), the second phase of the NIH HMP, aims to study the interactions by analyzing microbiome and host activities in longitudinal studies of disease-specific cohorts and by creating integrated data sets of microbiome and host functional properties (The Integrative HMP (iHMP) Research Network Consortium ), ultimately allowing us to analyze host and microbial DNA (genome) and RNA (transcriptome) sequences (Morgan and Huttenhower ). However, in the HMP study, the main anatomic sites where samples are collected are skin, mouth, nose, colon and vagina (ElRakaiby et al. ). So far as we are aware, these projects do not focus on the blood microbiome (which is probably unsurprising when most commentators assume that it does not exist).

The gut microbiome is by far the largest numerically, and our purpose here is not to review it in any detail, since this has been done very well in terms of its constitution (Lozupone et al.; Weinstock ),temporal variation (Caporaso et al.; Flores et al.; Thaiss et al. ),changes associated with diet (Muegge et al. ),obesity (Turnbaugh et al., ),age and geography (Delzenne and Cani; Delzenne et al.; Yatsunenko et al. ),inflammation (Cani et al., ),the immune system (Kau et al.; McDermott and Huffnagle )and various pathologies (Pflughoeft and Versalovic; Schulz et al. ).

its constitution (Lozupone et al.; Weinstock ),

temporal variation (Caporaso et al.; Flores et al.; Thaiss et al. ),

changes associated with diet (Muegge et al. ),

obesity (Turnbaugh et al., ),

age and geography (Delzenne and Cani; Delzenne et al.; Yatsunenko et al. ),

inflammation (Cani et al., ),

the immune system (Kau et al.; McDermott and Huffnagle )

and various pathologies (Pflughoeft and Versalovic; Schulz et al. ).

It was implied that a better understanding of microbiome-encoded pathways for xenobiotic metabolism might also have implications for improving the efficacy of pharmacologic interventions with neuromodulatory agents (Gonzalez et al. ), and that the exploration of microbiome and metagenome might give us insightful new perspectives regarding human genetics and how the microbiota contribute to immunity, as well as to metabolic and inflammatory diseases (Cho and Blaser; Blaser et al.; Blaser; Leslie and Young ). This is because it is assumed in such studies that it is the small-molecule products of the gut microbiome that can appear in the human serum metabolome, and thus influence the rest of the human body (e.g. Wikoff et al.; Holmes et al.; Le Chatelier et al., and see Table 2). Here we also need to mention lipopolysaccharide (LPS), a main constituent of the Gram-negative outer membrane that induces the production of cytokines and/or chemokines, which in turn regulate inflammatory and innate and subsequent adaptive immune responses (Glaros et al.; Rhee; Ronco ). The release of LPS may therefore change gut homeostasis, may play a role in e.g. inflammatory bowel disease and necrotizing enterocolitis (Rhee ), and may certainly act as an acute phase protein in sepsis (Ding and Jin ).

By contrast, our theme here is that it is additionally the microbes themselves that can pass from the gut (and other ‘external’ surfaces) into the human body, a phenomenon sometimes known as ‘dysbiosis’, albeit this term is more commonly used with another meaning. We here need to discriminate a changed (pathologic) microbiota in the place of origin from the results of a translocation of microbiota to other areas of the body. In the following sections, we use the term dysbiosis to describe changes in a microbiome in its main origin (typically the gut), and we coin the term ‘atopobiosis’ to describe microbes that appear in places other than where they should be.

The origin of detectable but non-proliferating microbes appears to be mainly via ‘atopobiosis’ of the gut microbiome

Dysbiosis, also known as dysbacteriosis, particularly referring to microbial imbalance in the digestive tract, has been widely discussed (e.g. Scher and Abramson; Scanlan et al.; Amar et al.; Bested, Logan and Selhub; Duytschaever et al.; Vaarala ). Core to this literature is the idea that factors that lead to significant changes in the gut microbiota composition (dysbiosis) ultimately result in pathology (Larsen et al.; Amar et al.,; Bested, Logan and Selhub; Burcelin et al.; De Angelis et al.; Fremont et al.; Lanter, Sauer and Davies; Petriz et al.; Power et al.; Tojo et al. ). Table 3 gives a list of diseases, largely inflammatory diseases, which have been associated with gut dysbiosis.

In addition, we argue here that as well as gut dysbiosis, a derangement of the gut microbiome, what we are seeing here, often called ‘translocation’ in the context of surgery (Swank and Deitch; MacFie ) and various diseases (Berg ) (see Table 4 that lists diseases and conditions where bacterial translocation is specifically implicated), is what might better be called atopobiosis (Greek ατoπoς or atopos, in the wrong place), i.e. an appearance of members of the gut (or other) microbiome in the wrong place. Bacterial translocation is therefore discussed in the context of the movement of gut origin microbes [that changed from normal (dysbiosis)] that moved across the ‘intact’ gastrointestinal tract into normally sterile tissues, including blood, where the organisms may then directly cause infection or inflammation leading to tissue injury, organ failure, etc. (Steinberg; Wiest and Rath; Balzan et al. ). We stress that they may be found in both infectious and non-infectious diseases as well as being translocated during surgery, and that atopobiosis of bacteria originating in the oral cavity, e.g. in periodontal disease, may also be significant in rheumatoid arthritis, for instance (see below). Fig. 3 provides a schematic representation of dysbiosis, bacterial translocation and atopobiosis.

How do gut bacteria escape into blood?

If the gut microbiome is seen as the main source of the blood microbiome, it is necessary to establish which kinds of conditions might permit this in the absence of real physical damage (as may, for instance, be caused by surgery) leading to microbial translocation. Wiest, Lawson and Geuking mention three possible points of entrance for bacteria into the surrounding (sterile) tissue: by dendritic cells via processes between epithelial cells, not affecting tight junction function,via injured/inflamed epithelium with dysfunctional epithelial barrier,and via M cells overlying Peyer's patches as specialized cells providing access of microbial products to antigen-presenting cells.

by dendritic cells via processes between epithelial cells, not affecting tight junction function,

via injured/inflamed epithelium with dysfunctional epithelial barrier,

and via M cells overlying Peyer's patches as specialized cells providing access of microbial products to antigen-presenting cells.

We discuss bacterial translocation in this context in the following sections.

The role of M cells and Peyer's patches in gut microbial translocation and atopobiosis

While the gut epithelium represents the largest mucosal tissue, the mechanisms underlying the interaction between the microbiome and the epithelial cells remain poorly understood (Mathias et al. ). Although this is a vast and complex field that warrants a review of its own, we briefly argue that gut dysbiosis results in an atypical interaction of both the microbiota, as well as their secretory products, with the gut epithelial layer. This results in an altered barrier function, which may also lead to changed mucosal immunity and ultimately to atopobiosis. The gut epithelium is necessarily normally quite impermeable to microbes, but there is increasing evidence that direct chemical communication between the microbiota and the epithelial cells regulates mucosal integrity (Venkatesh et al. ). A possible point of entry is by direct cellular uptake, and there is one type of cell that can take up microbes, and these are the M cells overlaying the Peyer's patches (Kernéis et al.; Jepson and Clark; Clark and Jepson; Corr, Gahan and Hill; Lelouard et al.; Fukuda, Hase and Ohno ). Peyer's patches are seen as the ‘immune sensors’ of the gut epithelium. Considerable evidence exists that they provide a primary route for the limited translocation of microbes between the gut epithelium and the blood system (Jung, Hugot and Barreau ). These interactions with the cells of the gut may suggest that changes in the intestinal microbiota also influence mucosal immunity (Sato, Kiyono and Fujihashi et al. ). This is indeed the case, and gut dysbiosis has been shown to play a significant role in the development of autoimmune diseases, in particular inflammatory bowel diseases (Clemente et al.; Morgan et al.; Hold et al.; Kostic, Xavier and Gevers; Owyang and Wu; Ma et al. ). It was also suggested that a changed gut microbiota represents the initial site of autoimmunity generation, and might be a critical epigenetic factor in autoimmune diseases such as rheumatoid arthritis (Scher and Abramson; Luckey et al.; Brusca, Abramson and Scher; Catrina, Deane and Scher; Cénit et al.; Taneja ). There is also evidence that regulatory T cells in the gut are influenced by microbial factors, and that a changed microbiota (dysbiosis) may influence the induction and suppressor functions of these cells, in turn leading to a changed gut mucosal immunity (Kinoshita and Takeda ).

We have earlier reviewed the literature that suggests that dysbiosis can cause gut epithelial barrier dysfunction, and thereby provide a point of entry into the body, including the blood, resulting in atopobiosis. This is supported by recent research that has suggested that blood microbiota might be implicated in various (cardiovascular and other) diseases. Sequence-based techniques provided evidence for the presence of such a blood microbiome. The question now arises as to whether such a microbiome's presence can be directly measured by e.g. ultrastructural (microscopic) methods, since a consequence of any translocation of microbes between the gut microbiome and blood is that they should then be observable in blood. The next sections will provide visual evidence of the presence of such a microbiota in Alzheimer's disease (AD) and PD. As shown in Table 3, these conditions are known to be associated with the presence of dysbiosis.

Direct measurement by ultrastructural (microscopic) methods

Direct measurement by ultrastructural (microscopic) methods of analysis shows that microbes are in fact common constituents of blood in inflammatory diseases [previously seen in PD—Fig. 8 in (Pretorius et al. and in AD—Fig. 2 in (Lipinski and Pretorius ). We show and annotate selected micrographs from these papers in Fig. 4]. An important concern that needs to be addressed, as is also the case with sequence-based methods, is whether the presence of microbiota in whole blood is indeed not the result of introduced external contamination. There is in fact considerable evidence in the literature that bacteria as well as other microorganisms can reside inside RBCs (e.g. Minasyan ), and thus able to cross the RBC membrane somehow (see Table 5). Transmission electron microscopy (TEM) analysis showing bacteria inside cells would also tend to imply that the bacteria were not externally introduced artefactually during the preparation of the samples.

For the current paper, we have revisited our AD and PD samples and figures from Pretorius et al. and Lipinski and Pretorius and noted the prevalence of bacteria in almost all of the AD and PD samples, in numbers much in excess of those seen in our database of thousands micrographs from healthy individuals. Here we show additional micrographs from the previously published samples (see Figs 5 and 6). In both conditions (see Figs 5AD and 6PD), microbes were noted in close proximity to RBCs, and in some cases RBCs extended pseudopodia-like projections towards the microbiota. SEM analysis of AD whole blood (Fig. 5) shows that mostly coccus-shaped bacteria are present. White blood cells are seen in close proximity to these bacteria in AD patients (see Fig. 5A–C). SEM analyses of PD patients (Fig. 6) show both coccus- and bacillus-shaped bacteria in close proximity to RBCs. We also observed that RBCs extend pseudopodia towards these bacteria and this might be part of the mechanism by which the bacteria enter the RBCs (see Fig. 6C–F). We also note possibly dividing coccus-shaped bacteria in both these conditions, indicated with blue arrows on Fig. 5A (AD patient) and Fig. 6D (PD patient). This might suggest that these bacteria may be(come) culturable under appropriate conditions (see also Soina et al.; Epstein ).

TEM analysis of the samples from Lipinski and Pretorius and Pretorius et al. showed the presence inside RBCs of cells that appeared to be microbial in nature (unpublished data). These internalized cells further provide evidence for a sustained presence of such a blood microbiota (and one hardly explained by contamination) (see Fig. 7A and B: AD and C and D: PD). Bacteria are shown with arrows in the micrographs. No bacterial membrane was noted; therefore, the bacteria may be L-forms. There seems to be bacterial species selectivity for a given disease, as our preliminary observations suggest a prevalence for bacillus-type bacteria in AD, but both coccus- and bacillus-shaped bacteria in PD patients.

Our observations suggest that the presence of bacteria in these two diseases occurs in only a small fraction of the RBC population, which is why we had not really noted them in our previous studies (e.g. Bester et al.; Pretorius et al.,,; Pretorius and Kell ), and SEM and TEM analysis confirms this observation. We have never (or not yet) found bacteria inside RBCs from healthy controls (these without overt, diagnosed diseases) when studying blood smears using TEM analysis. The microscopy preparation methods involve a washing process, and this may wash away some of the bacteria, or RBCs and white blood cells associated with bacteria. Therefore, the actual quantification of the bacteria can only be done by other means; however, dormancy and viability versus non-viability issues pertain (as discussed above).

We found a definite association between RBCs and bacteria, with RBCs (see Figs 6 and 7) forming pseudopodia-like extension, as if in the process of engulfing bacteria. Both coccoid (round) and bacillary (elongated) bacteria were found in PD whole blood SEM micrographs, but only coccoid forms in AD whole blood SEM micrographs. Samples from 25 diagnosed AD patients were studied and bacteria were detected in 14 individuals from this AD sample, while samples from 30 PD patients were studied, in 21 of whom we detected bacteria. Obviously, the type of bacteria cannot be identified from ultrastructural observations. As with the timeline of established cases such as the role of H. pylori in ulcers and colon cancer, the next tasks are to bring these microscopically observed bacteria into culture and to carry out sequence-based studies to establish their role (if any) in non-communicable diseases. However, to illustrate that the bacteria may indeed be engulfed by the RBCs, and to confirm that the phenomenon is not due to external contamination, we show TEM micrographs from both of the studied diseases (see Fig. 7, AD and PD).

CONCLUDING REMARKS AND PROSPECTIVE EXPERIMENTS

‘Non-culturable’ (which should be called ‘not-easily-culturable’ or ‘not-yet-cultured’) microbes are commonplace in the ‘environmental microbiology’ of soil and water, and the blood certainly represents an ‘environment’. As we show here, there is a large and scattered literature, increasing in size, to the effect that there might be a (mainly dormant) microbial component in a variety of chronic diseases that are normally considered to be non-microbial or non-communicable in nature, even when microbes appear absent by culturability criteria. Our previous work (e.g. Bester et al.; Pretorius et al.,; Kell and Pretorius,; Pretorius and Kell ) has implied iron dysregulation as a regular accompaniment to, and probable contributory factor for, a variety of similar diseases, all of which have an inflammatory component. We argue here that there is also a microbial contribution to this in the blood, and it is not unreasonable that the microbial requirement for iron means that, despite the oxidative stress it can entail (Touati; Kell, ), microbes may be anticipated to increase in prevalence when iron is free (e.g. Ratledge; Clifton, Corrent and Strong; Sia, Allred and Raymond; Chu et al. ) and available (D'Onofrio et al. ), probably behaving in a social manner (Kell, Kaprelyants and Grafen; West and Buckling; Diggle et al.; Harrison and Buckling ).

We have here pointed up the likelihood of a steady crop of effectively dormant microbes being a feature of blood biology in chronically diseased humans, including those with non-communicable diseases. As with any complex system, the magnitude of any component is affected by the kinetics of every relevant step; while the precise nature of all the interactions is uncertain, Fig. 8 describes the general network—the first step in any systems analysis (Kell; Kell and Knowles ).

Consequently, we recognize that the analysis above has largely been qualitative (the ‘presence’ of a microbial component in a specific disease is a qualitative statement). However, chronic, non-communicable diseases are very far from being static (and thousands of human genes change their expression at least 2-fold even on a diurnal basis; Zhang et al. ). Thus, a clear further issue is to seek to understand how the blood microbiome may co-vary with the day-to-day dynamics of chronic diseases. For example, rheumatoid arthritis has circadian rhythms (Straub and Cutolo ) and is well known to provide significant variations (‘flares’; Flurey et al. ) in severity at different times. A reasonable strategy is thus to look for changes in a detectable blood microbiome in this and other diseases that show such flares. As with H. pylori and stomach ulcers (and cancer), the simple prediction is that bactericidal antibiotics should be of value in the treatment of such supposedly non-communicable diseases. Indeed, this prediction is borne out for diseases such as rheumatoid arthritis (Ogrendik,; Kwiatkowska and Maślińska ) and multiple sclerosis (Ochoa-Repáraz et al.; ), while antipneumococcal vaccination has shown efficacy in preventing stroke (Vila-Corcoles et al. ). Of course, events such as heart attacks and strokes (and see Table 4) may also be seen as sudden increases in severity of an underlying condition, and in some cases (such as the much increased likelihood of strokes after subarachnoid haemorrhages; McMahon et al. ), analysis of changes in the blood microbiome might prove predictive.

The obvious next tasks are thus to relate the number and nature of blood microbes observed in cases such as the above to microbial sequences and antigens that can be detected in aliquots of the same samples (e.g. Salipante et al., ), to determine the physiological state of the various microbes (including e.g. whether they are L-forms), and to establish methods to bring them (back) into culture. Since microbes, inflammation and various syndromes are such common co-occurrences (as are coagulopathies; Kell and Pretorius ), longitudinal studies will have a specially important role, as they will both show the dynamics and be able to help discriminate cause and effect during the time evolution of chronic, non-communicable diseases in ageing populations. The immunogenicity of persisters, and their ability to induce various kinds of inflammation, must be rather different from that of replicating organisms, and this must be investigated. Armed with such collective knowledge, we might be better placed to develop therapeutics such as pre- and probiotics and bactericidal antibiotics for use in such cases previously thought to lack a microbial contribution.

FUNDING

We thank the Biotechnology and Biological Sciences Research Council (grant BB/L025752/1) as well as the National Research Foundation (NRF) of South Africa for supporting this collaboration.

Conflict of interest. None declared.

GLOSSARY

16S ribosomal RNA: a component of the 30S small subunit of prokaryotic ribosomes. The 16S rRNA gene is found in all bacteria and archaea and consists of nine short hypervariable regions that may be used to distinguish bacterial taxa.

Anabiosis: when an organism is in a state of very low metabolic activity to the extent where it is hardly measurable and in some cases come to a standstill. The physiological and biochemical processes are arrested for different periods of time but can be reversed.

Atopobiosis (Greek or atopos) appearance of the gut or other microbiome in the wrong place.

Bacterial translocation: the passage of viable resident bacteria from the gastrointestinal tract to normally sterile tissues such as the mesenteric lymph nodes and the other internal organs.

Cryptobiosis: refers to latent life or a state where an organism lacks any visible signs of life but is not dead in that it may revert to a state of aliveness as usually defined. Its metabolic activity becomes hardly measurable, or comes reversibly to a standstill.

Culturability: the ability of a cell to reproduce.

Direct viable count: the original method comprises incubation of samples with nutrients (yeast extract) and a single antimicrobial agent that specifically inhibits DNA synthesis but not RNA synthesis (nalidixic acid). Cell division ceases as a result of DNA synthesis inhibition but other cellular metabolic activities remain unaffected and therefore cells continue to metabolize nutrients and grow in size, which allows their detection microscopically in situ.

Dormant: not viable in the sense of not being more or less immediately culturable, but may be returned to a state of viability or culturability by preincubation under suitable conditions.

Dysbiosis: derangement of the species distribution in the normal microbiome.

L-forms: these bacteria are cell wall-deficient forms of normal bacteria. They are able to proliferate as sphaeroplasts or protoplasts under certain conditions.

Metagenomics: direct genetic analysis of a collection of genomes contained in an environmental sample.

Microbiome: the genetic sum of the ecological community of commensal, symbiotic and pathogenic microorganisms that lives on and inside our bodies.

‘Most Probable Number’ technique: is a method used to quantify the concentration of viable microorganisms in a sample. It involves replicate liquid broth growth in 10-fold dilutions. When a dilution lacks growth, it is assumed not to have any organisms. Back-calculation via a Poissonian distribution leads to the ‘most probable number’ in the original sample

Non-axenic culture: contains more than one species, variety or strain of organism.

Non-viable: incapable of observable replication by any stated means normally capable of effecting replication in the relevant organism.

Phylogenetics: a discipline of evolutionary biology that studies the relationships between organisms based on how closely similar some of their macromolecular sequences are.

Pleomorphic: possessing the ability to change shape or size in response to environmental stimuli.

Resuscitation: induction of apparently non-culturable cells to a state of culturability.

Sterile: refers to an absence of operationally viable organisms.

Viable: capable of observable replication, i.e. culturable, by any stated means.

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    Delzenne NM, Cani PD. Interaction between obesity and the gut microbiota: relevance in nutrition. Annu Rev Nutr. 2011;31:15-31.

    Not in our library10.1146/annurev-nutr-072610-145146

  82. 82.

    Delzenne NM, Neyrinck AM, Bäckhed F, et al. Targeting gut microbiota in obesity: effects of prebiotics and probiotics. Nat Rev Endocrinol. 2011;7:639-46.

    Not in our library10.1038/nrendo.2011.126

  83. 83.

    Demoruelle MK, Deane KD, Holers VM. When and where does inflammation begin in rheumatoid arthritis? Curr Opin Rheumatol. 2014;26:64-71.

    Not in our library10.1097/bor.0000000000000017

  84. 84.
    The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism · 2013
    Not checked
  85. 85.

    Desbonnet L, Garrett L, Clarke G, et al. The probiotic Bifidobacteria infantis: an assessment of potential antidepressant properties in the rat. J Psychiatr Res. 2008;43:164-74.

    Not in our library10.1016/j.jpsychires.2008.03.009

  86. 86.

    Detert J, Pischon N, Burmester GR, et al. The association between rheumatoid arthritis and periodontal disease. Arthritis Res Ther. 2010;12:218.

    Not in our library10.1186/ar3106

  87. 87.

    Devaraj S, Hemarajata P, Versalovic J. The human gut microbiome and body metabolism: implications for obesity and diabetes. Clin Chem. 2013;59:617-28.

    Not in our library10.1373/clinchem.2012.187617

  88. 88.

    Devine KM. Bacterial L-forms on tap: an improved methodology to generate Bacillus subtilis L-forms heralds a new era of research. Mol Microbiol. 2012;83:10-3.

    Not in our library10.1111/j.1365-2958.2011.07922.x

  89. 89.

    Didelot X, Bowden R, Wilson DJ, et al. Transforming clinical microbiology with bacterial genome sequencing. Nat Rev Genet. 2012;13:601-12.

    Not in our library10.1038/nrg3226

  90. 90.

    Diggle SP, Griffin AS, Campbell GS, et al. Cooperation and conflict in quorum-sensing bacterial populations. Nature. 2007;450:411-4.

    Not in our library10.1038/nature06279

  91. 91.
    Elevated Levels of Circulating DNA in Cardiovascular Disease Patients: Metagenomic Profiling of Microbiome in the Circulation · 2014
    No notice
  92. 92.

    Ding PH, Jin LJ. The role of lipopolysaccharide-binding protein in innate immunity: a revisit and its relevance to oral/periodontal health. J Periodontal Res. 2014;49:1-9.

    Not in our library10.1111/jre.12081

  93. 93.

    Ding T, Schloss PD. Dynamics and associations of microbial community types across the human body. Nature. 2014;509:357-60.

    Not in our library10.1038/nature13178

  94. 94.

    Domingue GJ. Demystifying pleomorphic forms in persistence and expression of disease: Are they bacteria, and is peptidoglycan the solution? Discov Med. 2010;10:234-46.

    Not in our library

  95. 95.

    Domingue GJ, Schlegel JU. Novel bacterial structures in human blood: cultural isolation. Infect Immun. 1977;15:621-7.

    Not in our library10.1128/iai.15.2.621-627.1977

  96. 96.

    Domingue GJ, Woody HB. Bacterial persistence and expression of disease. Clin Microbiol Rev. 1997;10:320-44.

    Not in our library10.1128/cmr.10.2.320

  97. 97.

    Domínguez-Cuevas P, Mercier R, Leaver M, et al. The rod to L-form transition of Bacillus subtilis is limited by a requirement for the protoplast to escape from the cell wall sacculus. Mol Microbiol. 2012;83:52-66.

    Not in our library10.1111/j.1365-2958.2011.07920.x

  98. 98.

    D'Onofrio A, Crawford JM, Stewart EJ, et al. Siderophores from neighboring organisms promote the growth of uncultured bacteria. Chem Biol. 2010;17:254-64.

    Not in our library10.1016/j.chembiol.2010.02.010

  99. 99.

    Dostal A, Baumgartner J, Riesen N, et al. Effects of iron supplementation on dominant bacterial groups in the gut, faecal SCFA and gut inflammation: a randomised, placebo-controlled intervention trial in South African children. Brit J Nutr. 2014;112:547-56.

    Not in our library10.1017/s0007114514001160

  100. 100.

    Dostal A, Chassard C, Hilty FM, et al. Iron depletion and repletion with ferrous sulfate or electrolytic iron modifies the composition and metabolic activity of the gut microbiota in rats. J Nutr. 2012;142:271-7.

    Not in our library10.3945/jn.111.148643

  101. 101.
    Survey of bacterial diversity in chronic wounds using Pyrosequencing, DGGE, and full ribosome shotgun sequencing · 2008
    No notice
  102. 102.

    Drennan M. What is ‘Sterile Blood’? Brit Med J. 1942;2:526.

    Not in our library

  103. 103.

    Duda VI, Suzina NE, Polivtseva VN, et al. Ultramicrobacteria: formation of the concept and contribution of ultramicrobacteria to biology. Mikrobiologiia. 2012;81:415-27.

    Not in our library

  104. 104.

    Duytschaever G, Huys G, Bekaert M, et al. Cross-sectional and longitudinal comparisons of the predominant fecal microbiota compositions of a group of pediatric patients with cystic fibrosis and their healthy siblings. Appl Environ Microb. 2011;77:8015-24.

    Not in our library10.1128/aem.05933-11

  105. 105.

    Duytschaever G, Huys G, Bekaert M, et al. Dysbiosis of bifidobacteria and Clostridium cluster XIVa in the cystic fibrosis fecal microbiota. J Cyst Fibros. 2013;12:206-15.

    Not in our library10.1016/j.jcf.2012.10.003

  106. 106.

    Ebringer A, Rashid T. Rheumatoid arthritis is caused by a Proteus urinary tract infection. APMIS. 2014;122:363-8.

    Not in our library10.1111/apm.12154

  107. 107.

    Eicher SC, Dehio C. Bartonella entry mechanisms into mammalian host cells. Cell Microbiol. 2012;14:1166-73.

    Not in our library10.1111/j.1462-5822.2012.01806.x

  108. 108.

    Eilers H, Pernthaler J, Glockner FO, et al. Culturability and In situ abundance of pelagic bacteria from the North Sea. Appl Environ Microb. 2000;66:3044-51.

    Not in our library10.1128/aem.66.7.3044-3051.2000

  109. 109.

    Eisenreich W, Dandekar T, Heesemann J, et al. Carbon metabolism of intracellular bacterial pathogens and possible links to virulence. Nat Rev Microbiol. 2010;8:401-12.

    Not in our library10.1038/nrmicro2351

  110. 110.

    Eleftheriadis T, Liakopoulos V, Leivaditis K, et al. Infections in hemodialysis: a concise review—Part 1: bacteremia and respiratory infections. Hippokratia. 2011;15:12-7.

    Not in our library

  111. 111.

    ElRakaiby M, Dutilh BE, Rizkallah MR, et al. Pharmacomicrobiomics: the impact of human microbiome variations on systems pharmacology and personalized therapeutics. Omics. 2014;18:402-14.

    Not in our library10.1089/omi.2014.0018

  112. 112.

    Emsley HC, Chamorro A. Stroke bugs: current and emerging concepts relevant to infection in cerebrovascular disease. Infect Disord Drug Targets. 2010;10:65-6.

    Not in our library

  113. 113.

    Emsley HC, Hopkins SJ. Acute ischaemic stroke and infection: recent and emerging concepts. Lancet Neurol. 2008;7:341-53.

    Not in our library10.1016/s1474-4422(08)70061-9

  114. 114.

    Emsley HC, Smith CJ, Gavin CM, et al. An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis. J Neuroimmunol. 2003;139:93-101.

    Not in our library10.1016/s0165-5728(03)00134-6

  115. 115.

    Emsley HC, Tyrrell PJ. Inflammation and infection in clinical stroke. J Cerebr Blood F Met. 2002;22:1399-419.

    Not in our library10.1097/01.wcb.0000037880.62590.28

  116. 116.

    Epstein SE, Zhou YF, Zhu J. Infection and atherosclerosis: emerging mechanistic paradigms. Circulation. 1999;100:e20-8.

    Not in our library10.1161/01.cir.100.4.e20

  117. 117.

    Epstein SE, Zhu J, Najafi AH, et al. Insights into the role of infection in atherogenesis and in plaque rupture. Circulation. 2009;119:3133-41.

    Not in our library10.1161/circulationaha.109.849455

  118. 118.

    Epstein SS. The phenomenon of microbial uncultivability. Curr Opin Microbiol. 2013;16:636-42.

    Not in our library10.1016/j.mib.2013.08.003

  119. 119.

    Erridge C. The roles of pathogen-associated molecular patterns in atherosclerosis. Trends Cardiovas Med. 2008;18:52-6.

    Not in our library10.1016/j.tcm.2007.12.003

  120. 120.
    L-form bacteria, cell walls and the origins of life · 2013
    No notice
  121. 121.

    Everard A, Matamoros S, Geurts L, et al. Saccharomyces boulardii administration changes gut microbiota and reduces hepatic steatosis, low-grade inflammation, and fat mass in obese and type 2 diabetic db/db mice. MBio. 2014;5:e01011-4.

    Not in our library10.1128/mbio.01011-14

  122. 122.

    Faure M, Mettraux C, Moennoz D, et al. Specific amino acids increase mucin synthesis and microbiota in dextran sulfate sodium-treated rats. J Nutr. 2006;136:1558-64.

    Not in our library10.1093/jn/136.6.1558

  123. 123.

    Feeley JC, Gorman GW, Weaver RE, et al. Primary isolation media for Legionnaires disease bacterium. J Clin Microbiol. 1978;8:320-5.

    Not in our library10.1128/jcm.8.3.320-325.1978

  124. 124.

    Fernández-Cruz A, Marin M, Kestler M, et al. The value of combining blood culture and SeptiFast data for predicting complicated bloodstream infections caused by Gram-positive bacteria or Candida species. J Clin Microbiol. 2013;51:1130-6.

    Not in our library10.1128/jcm.02882-12

  125. 125.

    Festi D, Schiumerini R, Eusebi LH, et al. Gut microbiota and metabolic syndrome. World J Gastroenterol. 2014;20:16079-94.

    Not in our library10.3748/wjg.v20.i43.16079

  126. 126.

    Finegold SM, Dowd SE, Gontcharova V, et al. Pyrosequencing study of fecal microflora of autistic and control children. Anaerobe. 2010;16:444-53.

    Not in our library10.1016/j.anaerobe.2010.06.008

  127. 127.
    Temporal variability is a personalized feature of the human microbiome · 2014
    No notice
  128. 128.

    Flurey CA, Morris M, Richards P, et al. It's like a juggling act: rheumatoid arthritis patient perspectives on daily life and flare while on current treatment regimes. Rheumatology. 2014;53:696-703.

    Not in our library10.1093/rheumatology/ket416

  129. 129.

    Fredricks DN. The Human Microbiota: How Microbial Communities Affect Health and Disease. 2013.

    Not in our library

  130. 130.

    Fremont M, Coomans D, Massart S, et al. High-throughput 16S rRNA gene sequencing reveals alterations of intestinal microbiota in myalgic encephalomyelitis/chronic fatigue syndrome patients. Anaerobe. 2013;22:50-6.

    Not in our library10.1016/j.anaerobe.2013.06.002

  131. 131.

    French AL, Evans CT, Agniel DM, et al. Microbial translocation and liver disease progression in women coinfected with HIV and hepatitis C virus. J Infect Dis. 2013;208:679-89.

    Not in our library10.1093/infdis/jit225

  132. 132.

    Fricke WF, Rasko DA. Bacterial genome sequencing in the clinic: bioinformatic challenges and solutions. Nat Rev Genet. 2014;15:49-55.

    Not in our library10.1038/nrg3624

  133. 133.

    Fugate JE, Lyons JL, Thakur KT, et al. Infectious causes of stroke. Lancet Infect Dis. 2014;14:869-80.

    Not in our library10.1016/s1473-3099(14)70755-8

  134. 134.

    Fukuda S, Hase K, Ohno H. Application of a mouse ligated Peyer's patch intestinal loop assay to evaluate bacterial uptake by M cells. J Vis Exp. 2011;e3225-30.

    Not in our library10.3791/3225

  135. 135.

    Gaibani P, Mariconti M, Bua G, et al. Development of a broad-range 23S rDNA real-time PCR assay for the detection and quantification of pathogenic bacteria in human whole blood and plasma specimens. Biomed Res Int. 2013;2013:264651.

    Not in our library10.1155/2013/264651

  136. 136.
    Metabolism of Cholesterol and Bile Acids by the Gut Microbiota · 2013
    No notice
  137. 137.

    Gerdes K, Maisonneuve E. Bacterial persistence and toxin-antitoxin loci. Annu Rev Microbiol. 2012;66:103-23.

    Not in our library10.1146/annurev-micro-092611-150159

  138. 138.

    Germain E, Castro-Roa D, Zenkin N, et al. Molecular mechanism of bacterial persistence by HipA. Mol Cell. 2013;52:248-54.

    Not in our library10.1016/j.molcel.2013.08.045

  139. 139.

    Gest H. The Modern Myth of ‘Unculturable’ Bacteria: Scotoma of Contemporary Microbiology. 2008.

    Not in our library

  140. 140.

    Geurts L, Neyrinck AM, Delzenne NM, et al. Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics. Benef Microbes. 2014;5:3-17.

    Not in our library10.3920/bm2012.0065

  141. 141.

    Giannelli V, DiGregorio V, Iebba V, et al. Microbiota and the gut-liver axis: bacterial translocation, inflammation and infection in cirrhosis. World J Gastroenterol. 2014;20:16795-810.

    Not in our library10.3748/wjg.v20.i45.16795

  142. 142.

    Gich F, Schubert K, Bruns A, et al. Specific detection, isolation, and characterization of selected, previously uncultured members of the freshwater bacterioplankton community. Appl Environ Microb. 2005;71:5908-19.

    Not in our library10.1128/aem.71.10.5908-5919.2005

  143. 143.

    Glaros TG, Chang S, Gilliam EA, et al. Causes and consequences of low grade endotoxemia and inflammatory diseases. Front Biosci. 2013;5:754-65.

    Not in our library10.2741/s405

  144. 144.

    Gonzalez A, Stombaugh J, Lozupone C, et al. The mind-body-microbial continuum. Dialogues Clin Neurosci. 2011;13:55-62.

    Not in our library10.31887/dcns.2011.13.1/agonzalez

  145. 145.

    Grau AJ, Urbanek C, Palm F. Common infections and the risk of stroke. Nat Rev Neurol. 2010;6:681-94.

    Not in our library10.1038/nrneurol.2010.163

  146. 146.

    Gribbin JR. In Search of Schrödinger's Cat: Quantum Physics and Reality. 1985.

    Not in our library

  147. 147.

    Grif K, Fille M, Würzner R, et al. Rapid detection of bloodstream pathogens by real-time PCR in patients with sepsis. Wien Klin Wochenschr. 2012a;124:266-70.

    Not in our library10.1007/s00508-012-0159-4

  148. 148.

    Grif K, Heller I, Prodinger WM, et al. Improvement of detection of bacterial pathogens in normally sterile body sites with a focus on orthopedic samples by use of a commercial 16S rRNA broad-range PCR and sequence analysis. J Clin Microbiol. 2012b;50:2250-4.

    Not in our library10.1128/jcm.00362-12

  149. 149.

    Groebel K, Hoelzle K, Wittenbrink MM, et al. Mycoplasma suis invades porcine erythrocytes. Infect Immun. 2009;77:576-84.

    Not in our library10.1128/iai.00773-08

  150. 150.

    Guo ZZ, Wang P, Yi ZH, et al. The crosstalk between gut inflammation and gastrointestinal disorders during acute pancreatitis. Curr Pharm Des. 2014;20:1051-62.

    Not in our library10.2174/13816128113199990414

  151. 151.

    Harrison F, Buckling A. Cooperative production of siderophores by Pseudomonas aeruginosa. Front Biosci. 2009;14:4113-26.

    Not in our library10.2741/3516

  152. 152.
    Duration of antibiotic therapy for bacteremia: a systematic review and meta-analysis · 2011
    No notice
  153. 153.

    Hevia A, Milani C, Lopez P, et al. Intestinal dysbiosis associated with systemic lupus erythematosus. MBio. 2014;5:e01548-14.

    Not in our library10.1128/mbio.01548-14

  154. 154.

    Hill MJ. Intestinal flora and endogenous vitamin synthesis. Eur J Cancer Prev. 1997;6(Suppl 1):S43-5.

    Not in our library10.1097/00008469-199703001-00009

  155. 155.

    Hold GL, Smith M, Grange C, et al. Role of the gut microbiota in inflammatory bowel disease pathogenesis: what have we learnt in the past 10 years? World J Gastroenterol. 2014;20:1192-210.

    Not in our library10.3748/wjg.v20.i5.1192

  156. 156.

    Holden DW. Microbiology. Persisters unmasked. Science. 2015;347:30-2.

    Not in our library10.1126/science.1262033

  157. 157.

    Holmes E, Li JV, Athanasiou T, et al. Understanding the role of gut microbiome-host metabolic signal disruption in health and disease. Trends Microbiol. 2011;19:349-59.

    Not in our library10.1016/j.tim.2011.05.006

  158. 158.

    Hopkins PN. Molecular biology of atherosclerosis. Physiol Rev. 2013;93:1317-542.

    Not in our library10.1152/physrev.00004.2012

  159. 159.

    Horzempa J, O'Dee DM, Stolz DB, et al. Invasion of erythrocytes by Francisella tularensis. J Infect Dis. 2011;204:51-9.

    Not in our library10.1093/infdis/jir221

  160. 160.

    Huang Y, Fan XG, Tang ZS, et al. Detection of Helicobacter pylori DNA in peripheral blood from patients with peptic ulcer or gastritis. APMIS. 2006;114:851-6.

    Not in our library10.1111/j.1600-0463.2006.apm_425.x

  161. 161.

    Hugenholtz P. Exploring prokaryotic diversity in the genomic era. Genome Biol. 2002;3:0003.1–0003.8.

    Not in our library10.1186/gb-2002-3-2-reviews0003

  162. 162.

    Isberg RR. Discrimination between intracellular uptake and surface adhesion of bacterial pathogens. Science. 1991;252:934-8.

    Not in our library10.1126/science.1674624

  163. 163.

    Iwaki-Egawa S, Ihler GM. Comparison of the abilities of proteins from Bartonella bacilliformis and Bartonella henselae to deform red cell membranes and to bind to red cell ghost proteins. FEMS Microbiol Lett. 1997;157:207-17.

    Not in our library10.1111/j.1574-6968.1997.tb12775.x

  164. 164.

    Jepson MA, Clark MA. Studying M cells and their role in infection. Trends Microbiol. 1998;6:359-65.

    Not in our library10.1016/s0966-842x(98)01337-7

  165. 165.

    Jiang W, Lederman MM, Hunt P, et al. Plasma levels of bacterial DNA correlate with immune activation and the magnitude of immune restoration in persons with antiretroviral-treated HIV infection. J Infect Dis. 2009;199:1177-85.

    Not in our library10.1086/597476

  166. 166.

    Joyce SA, MacSharry J, Casey PG, et al. Regulation of host weight gain and lipid metabolism by bacterial bile acid modification in the gut. P Natl Acad Sci USA. 2014;111:7421-6.

    Not in our library10.1073/pnas.1323599111

  167. 167.

    Jun DW, Kim KT, Lee OY, et al. Association between small intestinal bacterial overgrowth and peripheral bacterial DNA in cirrhotic patients. Dig Dis Sci. 2010;55:1465-71.

    Not in our library10.1007/s10620-009-0870-9

  168. 168.
    Peyer's Patches: The Immune Sensors of the Intestine · 2010
    No notice
  169. 169.

    Kahle K, Kraus M, Scheppach W, et al. Studies on apple and blueberry fruit constituents: do the polyphenols reach the colon after ingestion? Mol Nutr Food Res. 2006;50:418-23.

    Not in our library10.1002/mnfr.200500211

  170. 170.

    Kakiyama G, Pandak WM, Gillevet PM, et al. Modulation of the fecal bile acid profile by gut microbiota in cirrhosis. J Hepatol. 2013;58:949-55.

    Not in our library10.1016/j.jhep.2013.01.003

  171. 171.

    Kamagata Y, Tamaki H. Cultivation of uncultured fastidious microbes. Microbes Environ. 2005;20:85-91.

    Not in our library

  172. 172.
    Reduced Incidence of Prevotella and Other Fermenters in Intestinal Microflora of Autistic Children · 2013
    No notice
  173. 173.

    Kaprelyants AS, Gottschal JC, Kell DB. Dormancy in non-sporulating bacteria. FEMS Microbiol Rev. 1993;10:271-85.

    Not in our library10.1111/j.1574-6968.1993.tb05871.x

  174. 174.

    Kaprelyants AS, Kell DB. Dormancy in stationary-phase cultures of Micrococcus luteus: flow cytometric analysis of starvation and resuscitation. Appl Environ Microb. 1993;59:3187-96.

    Not in our library10.1128/aem.59.10.3187-3196.1993

  175. 175.

    Kaprelyants AS, Mukamolova GV, Davey HM, et al. Quantitative analysis of the physiological heterogeneity within starved cultures of Micrococcus luteus by flow cytometry and cell sorting. Appl Environ Microb. 1996;62:1311-6.

    Not in our library10.1128/aem.62.4.1311-1316.1996

  176. 176.

    Kaprelyants AS, Mukamolova GV, Kell DB. Estimation of dormant Micrococcus luteus cells by penicillin lysis and by resuscitation in cell-free spent medium at high dilution. FEMS Microbiol Lett. 1994;115:347-52.

    Not in our library

  177. 177.

    Kaprelyants AS, Mukamolova GV, Kormer SS, et al. Intercellular signalling and the multiplication of prokaryotes: bacterial cytokines. Symp Soc Gen Microbi. 1999;57:33-69.

    Not in our library

  178. 178.

    Karlsson FH, Fak F, Nookaew I, et al. Symptomatic atherosclerosis is associated with an altered gut metagenome. Nat Commun. 2012;3:1245.

    Not in our library10.1038/ncomms2266

  179. 179.

    Karlsson FH, Tremaroli V, Nookaew I, et al. Gut metagenome in European women with normal, impaired and diabetic glucose control. Nature. 2013;498:99-103.

    Not in our library10.1038/nature12198

  180. 180.

    Karri S, Martinez VA, Coimbatore G. Effect of dihydrotestosterone on gastrointestinal tract of male Alzheimer's disease transgenic mice. 2010;48:453-65.

    Not in our library

  181. 181.

    Kau AL, Ahern PP, Griffin NW, et al. Human nutrition, the gut microbiome and the immune system. Nature. 2011;474:327-36.

    Not in our library10.1038/nature10213

  182. 182.

    Keilin D. The problem of anabiosis or latent life: history and current concept. P Roy Soc Lond B Bio. 1959;150:149-91.

    Not in our library10.1098/rspb.1959.0013

  183. 183.

    Kell DB. Metabolomics, modelling and machine learning in systems biology: towards an understanding of the languages of cells. The 2005 Theodor Bücher lecture. FEBS J. 2006;273:873-94.

    Not in our library10.1111/j.1742-4658.2006.05136.x

  184. 184.
    Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases · 2009
    No notice
  185. 185.

    Kell DB. Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson's, Huntington's, Alzheimer's, prions, bactericides, chemical toxicology and others as examples. Arch Toxicol. 2010;84:825-89.

    Not in our library10.1007/s00204-010-0577-x

  186. 186.

    Kell DB, Kaprelyants AS, Grafen A. Pheromones, social behaviour and the functions of secondary metabolism in bacteria. Trends Ecol Evol. 1995;10:126-9.

    Not in our library10.1016/s0169-5347(00)89013-8

  187. 187.

    Kell DB, Kaprelyants AS, Weichart DH, et al. Viability and activity in readily culturable bacteria: a review and discussion of the practical issues. Anton Leeuw. 1998;73:169-87.

    Not in our library10.1023/a:1000664013047

  188. 188.

    Kell DB, Knowles JD, Szallasi Z, Stelling J, Periwal V. The role of modeling in systems biology. System Modeling in Cellular Biology: From Concepts to Nuts and Bolts. 2006;3-18.

    Not in our library

  189. 189.

    Kell DB, Mukamolova GV, Finan CL, Bull AT, et al. Resuscitation of ‘uncultured’ microorganisms. Microbial Diversity and Bioprospecting. 2003;100-8.

    Not in our library

  190. 190.
    How drugs get into cells: tested and testable predictions to help discriminate between transporter-mediated uptake and lipoidal bilayer diffusion · 2014
    No notice
  191. 191.

    Kell DB, Pretorius E. Serum ferritin is an important inflammatory disease marker, as it is mainly a leakage product from damaged cells. Metallomics. 2014;4:748-73.

    Not in our library10.1039/c3mt00347g

  192. 192.

    Kell DB, Pretorius E. The simultaneous occurrence of both hypercoagulability and hypofibrinolysis in blood and serum during systemic inflammation, and the roles of iron and fibrin(ogen). Integr Biol. 2015;7:24-52.

    Not in our library10.1039/c4ib00173g

  193. 193.

    Kell DB, Ryder HM, Kaprelyants AS, et al. Quantifying heterogeneity: flow cytometry of bacterial cultures. Anton Leeuw. 1991;60:145-58.

    Not in our library10.1007/bf00430362

  194. 194.

    Keller M, Zengler K. Tapping into microbial diversity. Nat Rev Microbiol. 2004;2:141-50.

    Not in our library10.1038/nrmicro819

  195. 195.

    Keren I, Kaldalu N, Spoering A, et al. Persister cells and tolerance to antimicrobials. FEMS Microbiol Lett. 2004a;230:13-8.

    Not in our library10.1016/s0378-1097(03)00856-5

  196. 196.

    Keren I, Shah D, Spoering A, et al. Specialized persister cells and the mechanism of multidrug tolerance in Escherichia coli. J Bacteriol. 2004b;186:8172-80.

    Not in our library10.1128/jb.186.24.8172-8180.2004

  197. 197.

    Kernéis S, Bogdanova A, Kraehenbuhl JP, et al. Conversion by Peyer's patch lymphocytes of human enterocytes into M cells that transport bacteria. Science. 1997;277:949-52.

    Not in our library10.1126/science.277.5328.949

  198. 198.

    Kibru D, Gelaw B, Alemu A, et al. Helicobacter pylori infection and its association with anemia among adult dyspeptic patients attending Butajira Hospital, Ethiopia. BMC Infect Dis. 2014;14:656.

    Not in our library10.1186/s12879-014-0656-3

  199. 199.

    Kimura I, Ozawa K, Inoue D, et al. The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. Nat Commun. 2013;4:1829.

    Not in our library10.1038/ncomms2852

  200. 200.

    Kinoshita M, Takeda K. Microbial and dietary factors modulating intestinal regulatory T cell homeostasis. FEBS Lett. 2014;588:4182-7.

    Not in our library10.1016/j.febslet.2014.03.018

  201. 201.

    Kishino S, Takeuchi M, Park S-B, et al. Polyunsaturated fatty acid saturation by gut lactic acid bacteria affecting host lipid composition. P Natl Acad Sci USA. 2013;110:17808-13.

    Not in our library10.1073/pnas.1312937110

  202. 202.

    Klatt NR, Funderburg NT, Brenchley JM. Microbial translocation, immune activation, and HIV disease. Trends Microbiol. 2013;21:6-13.

    Not in our library10.1016/j.tim.2012.09.001

  203. 203.

    Kocan KM, de la Fuente J, Blouin EF, et al. Anaplasma marginale (Rickettsiales: Anaplasmataceae): recent advances in defining host-pathogen adaptations of a tick-borne rickettsia. Parasitology. 2004;129(Suppl):285-300.

    Not in our library10.1017/s0031182003004700

  204. 204.

    Koch AL. The adaptive responses of Escherichia coli to a feast and famine existence. Adv Microb Physiol. 1971;6:147-217.

    Not in our library10.1016/s0065-2911(08)60069-7

  205. 205.

    Koch AL, Neidhardt FC, et al. The variability and individuality of the bacterium. Escherichia coli and Salmonella Typhimurium: Cellular and Molecular Biology. 1987;1606-14.

    Not in our library

  206. 206.

    Koeth RA, Wang Z, Levison BS, et al. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med. 2013;19:576-85.

    Not in our library10.1038/nm.3145

  207. 207.

    Kogure K, Simidu U, Taga N. A tentative direct microscopic method for counting living marine bacteria. Can J Microbiol. 1979;25:415-20.

    Not in our library10.1139/m79-063

  208. 208.
    A Guide to Enterotypes across the Human Body: Meta-Analysis of Microbial Community Structures in Human Microbiome Datasets · 2013
    No notice
  209. 209.

    Koren O, Spor A, Felin J, et al. Human oral, gut, and plaque microbiota in patients with atherosclerosis. P Natl Acad Sci USA. 2011;108:4592-8.

    Not in our library10.1073/pnas.1011383107

  210. 210.

    Kostic AD, Xavier RJ, Gevers D. The microbiome in inflammatory bowel disease: current status and the future ahead. Gastroenterology. 2014;146:1489-99.

    Not in our library10.1053/j.gastro.2014.02.009

  211. 211.

    Kotsaki A, Giamarellos-Bourboulis EJ. Emerging drugs for the treatment of sepsis. Expert Opin Emerg Dr. 2012;17:379-91.

    Not in our library10.1517/14728214.2012.697151

  212. 212.

    Kozarov E, Sweier D, Shelburne C, et al. Detection of bacterial DNA in atheromatous plaques by quantitative PCR. Microbes Infect. 2006;8:687-93.

    Not in our library10.1016/j.micinf.2005.09.004

  213. 213.
    The Link Between Periodontal Disease and Rheumatoid Arthritis: An Updated Review · 2014
    No notice
  214. 214.

    Kwiatkowska B, Maślińska M. Macrolide therapy in chronic inflammatory diseases. Mediat Inflamm. 2012;2012:636157.

    Not in our library10.1155/2012/636157

  215. 215.
    Genomic Encyclopedia of Bacteria and Archaea: Sequencing a Myriad of Type Strains · 2014
    No notice
  216. 216.

    Lagier JC, Edouard S, Pagnier I, et al. Current and past strategies for bacterial culture in clinical microbiology. Clin Microbiol Rev. 2015a;28:208-36.

    Not in our library10.1128/cmr.00110-14

  217. 217.

    Lagier JC, Hugon P, Khelaifia S, et al. The rebirth of culture in microbiology through the example of culturomics to study human gut microbiota. Clin Microbiol Rev. 2015b;28:237-64.

    Not in our library10.1128/cmr.00014-14

  218. 218.

    Lanter BB, Sauer K, Davies DG. Bacteria present in carotid arterial plaques are found as biofilm deposits which may contribute to enhanced risk of plaque rupture. MBio. 2014;5:e01206-14.

    Not in our library10.1128/mbio.01206-14

  219. 219.
    Gut Microbiota in Human Adults with Type 2 Diabetes Differs from Non-Diabetic Adults · 2010
    No notice
  220. 220.

    Lasken RS. Genomic sequencing of uncultured microorganisms from single cells. Nat Rev Microbiol. 2012;10:631-40.

    Not in our library10.1038/nrmicro2857

  221. 221.

    Lasken RS, McLean JS. Recent advances in genomic DNA sequencing of microbial species from single cells. Nat Rev Genet. 2014;15:577-84.

    Not in our library10.1038/nrg3785

  222. 222.

    Le Chatelier E, Nielsen T, Qin J, et al. Richness of human gut microbiome correlates with metabolic markers. Nature. 2013;500:541-6.

    Not in our library10.1038/nature12506

  223. 223.

    LeBlanc JG, Milani C, de Giori GS, et al. Bacteria as vitamin suppliers to their host: a gut microbiota perspective. Curr Opin Biotechnol. 2013;24:160-8.

    Not in our library10.1016/j.copbio.2012.08.005

  224. 224.

    Leli C, Cardaccia A, Ferranti M, et al. Procalcitonin better than C-reactive protein, erythrocyte sedimentation rate, and white blood cell count in predicting DNAemia in patients with sepsis. Scand J Infect Dis. 2014;46:745-52.

    Not in our library10.3109/00365548.2014.936493

  225. 225.

    Lelouard H, Henri S, De Bovis B, et al. Pathogenic bacteria and dead cells are internalized by a unique subset of Peyer's patch dendritic cells that express lysozyme. Gastroenterology. 2010;138:173-84.

    Not in our library10.1053/j.gastro.2009.09.051

  226. 226.

    Leslie JL, Young VB. The rest of the story: the microbiome and gastrointestinal infections. Curr Opin Microbiol. 2015;23c:121-5.

    Not in our library10.1016/j.mib.2014.11.010

  227. 227.

    Lewis K. Persister cells. Annu Rev Microbiol. 2010;64:357-72.

    Not in our library10.1146/annurev.micro.112408.134306

  228. 228.

    Lin W, Weinberg EM, Chung RT. Pathogenesis of accelerated fibrosis in HIV/HCV co-infection. J Infect Dis. 2013;207(Suppl 1):S13-8.

    Not in our library10.1093/infdis/jis926

  229. 229.

    Ling LL, Schneider T, Peoples AJ, et al. A new antibiotic kills pathogens without detectable resistance. Nature. 2015;517:455-9.

    Not in our library10.1038/nature14098

  230. 230.

    Lipinski B, Pretorius E. The role of iron-induced fibrin in the pathogenesis of Alzheimer's disease and the protective role of magnesium. Front Hum Neurosci. 2013;7:735.

    Not in our library10.3389/fnhum.2013.00735

  231. 231.

    Loman NJ, Constantinidou C, Chan JZ, et al. High-throughput bacterial genome sequencing: an embarrassment of choice, a world of opportunity. Nat Rev Microbiol. 2012;10:599-606.

    Not in our library10.1038/nrmicro2850

  232. 232.

    Lozupone CA, Li M, Campbell TB, et al. Alterations in the gut microbiota associated with HIV-1 infection. Cell Host Microbe. 2013;14:329-39.

    Not in our library10.1016/j.chom.2013.08.006

  233. 233.

    Lozupone CA, Stombaugh JI, Gordon JI, et al. Diversity, stability and resilience of the human gut microbiota. Nature. 2012;489:220-30.

    Not in our library10.1038/nature11550

  234. 234.

    Luckey D, Gomez A, Murray J, et al. Bugs, us: the role of the gut in autoimmunity. Indian J Med Res. 2013;138:732-43.

    Not in our library

  235. 235.

    Lysak LV, Lapygina EV, Konova IA, et al. Quantity and taxonomic composition of ultramicrobacteria in soils. Microbiology. 2010;79:408-12.

    Not in our library

  236. 236.

    Ma HD, Wang YH, Chang C, et al. The intestinal microbiota and microenvironment in liver. Autoimmun Rev. 2015;14:183-91.

    Not in our library10.1016/j.autrev.2014.10.013

  237. 237.

    McColl BW, Allan SM, Rothwell NJ. Systemic infection, inflammation and acute ischemic stroke. Neuroscience. 2009;158:1049-61.

    Not in our library10.1016/j.neuroscience.2008.08.019

  238. 238.

    McDermott AJ, Huffnagle GB. The microbiome and regulation of mucosal immunity. Immunology. 2014;142:24-31.

    Not in our library10.1111/imm.12231

  239. 239.

    Macdonell MT, Hood MA. Isolation and characterization of ultramicrobacteria from a gulf coast estuary. Appl Environ Microb. 1982;43:566-71.

    Not in our library10.1128/aem.43.3.566-571.1982

  240. 240.

    MacFie J. Current status of bacterial translocation as a cause of surgical sepsis. Brit Med Bull. 2004;71:1-11.

    Not in our library10.1093/bmb/ldh029

  241. 241.
    HIV Infection is associated with compositional and functional shifts in the rectal mucosal microbiota · 2013
    No notice
  242. 242.

    Macintire DK, Bellhorn TL. Bacterial translocation: clinical implications and prevention. Vet Clin N Am-Small. 2002;32:1165-78.

    Not in our library10.1016/s0195-5616(02)00037-2

  243. 243.

    McLaughlin RW, Vali H, Lau PCK, et al. Are there naturally occurring pleomorphic bacteria in the blood of healthy humans? J Clin Microbiol. 2002;40:4771-5.

    Not in our library10.1128/jcm.40.12.4771-4775.2002

  244. 244.

    McMahon CJ, Hopkins S, Vail A, et al. Inflammation as a predictor for delayed cerebral ischemia after aneurysmal subarachnoid haemorrhage. J Neurointerv Surg. 2013;5:512-7.

    Not in our library10.1136/neurintsurg-2012-010386

  245. 245.

    Madan JC, Koestler DC, Stanton BA, et al. Serial analysis of the gut and respiratory microbiome in cystic fibrosis in infancy: interaction between intestinal and respiratory tracts and impact of nutritional exposures. MBio. 2012;3:e00251–12.

    Not in our library10.1128/mbio.00251-12

  246. 246.

    Maisonneuve E, Castro-Camargo M, Gerdes K. (p)ppGpp controls bacterial persistence by stochastic induction of toxin-antitoxin activity. Cell. 2013;154:1140-50.

    Not in our library10.1016/j.cell.2013.07.048

  247. 247.

    Maisonneuve E, Gerdes K. Molecular mechanisms underlying bacterial persisters. Cell. 2014;157:539-48.

    Not in our library10.1016/j.cell.2014.02.050

  248. 248.

    Maiwald M, Relman DA. Whipple's disease and Tropheryma whippelii: secrets slowly revealed. Clin Infect Dis. 2001;32:457-63.

    Not in our library10.1086/318512

  249. 249.

    Maiwald M, von Herbay A, Fredricks DN, et al. Cultivation of Tropheryma whipplei from cerebrospinal fluid. J Infect Dis. 2003;188:801-8.

    Not in our library10.1086/378073

  250. 250.

    Malaguarnera G, Giordano M, Nunnari G, et al. Gut microbiota in alcoholic liver disease: pathogenetic role and therapeutic perspectives. World J Gastroenterol. 2014;20:16639-48.

    Not in our library10.3748/wjg.v20.i44.16639

  251. 251.

    Mancini N, Carletti S, Ghidoli N, et al. The era of molecular and other non-culture-based methods in diagnosis of sepsis. Clin Microbiol Rev. 2010;23:235-51.

    Not in our library10.1128/cmr.00043-09

  252. 252.

    Manichanh C, Borruel N, Casellas F, et al. The gut microbiota in IBD. Nat Rev Gastroentero. 2012;9:599-608.

    Not in our library10.1038/nrgastro.2012.152

  253. 253.
    Bioavailability of Dietary Polyphenols and Gut Microbiota Metabolism: Antimicrobial Properties · 2015
    No notice
  254. 254.

    Mariotti S, Pardini M, Gagliardi MC, et al. Dormant Mycobacterium tuberculosis fails to block phagosome maturation and shows unexpected capacity to stimulate specific human T lymphocytes. J Immunol. 2013;191:274-82.

    Not in our library10.4049/jimmunol.1202900

  255. 255.

    Marshall B. Helicobacter connections. ChemMedChem. 2006;1:783-802.

    Not in our library10.1002/cmdc.200600153

  256. 256.

    Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1984;1:1311-5.

    Not in our library10.1016/s0140-6736(84)91816-6

  257. 257.

    Martin F-PJ, Dumas M-E, Wang Y, et al. A top-down systems biology view of microbiome-mammalian metabolic interactions in a mouse model. Mol Syst Biol. 2007;3:112.

    Not in our library10.1038/msb4100153

  258. 258.

    Martínez I, Perdicaro DJ, Brown AW, et al. Diet-induced alterations of host cholesterol metabolism are likely to affect the gut microbiota composition in hamsters. Appl Environ Microb. 2013;79:516-24.

    Not in our library10.1128/aem.03046-12

  259. 259.

    Martínez I, Wallace G, Zhang C, et al. Diet-induced metabolic improvements in a hamster model of hypercholesterolemia are strongly linked to alterations of the gut microbiota. Appl Environ Microb. 2009;75:4175-84.

    Not in our library10.1128/aem.00380-09

  260. 260.

    Maslowski KM, Vieira AT, Ng A, et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43. Nature. 2009;461:1282-6.

    Not in our library10.1038/nature08530

  261. 261.

    Mason CA, Hamer G, Bryers JD. The death and lysis of microorganisms in environmental processes. FEMS Microbiol Rev. 1986;39:373-401.

    Not in our library

  262. 262.

    Mathias A, Pais B, Favre L, et al. Role of secretory IgA in the mucosal sensing of commensal bacteria. Gut Microbes. 2014;5:688-95.

    Not in our library10.4161/19490976.2014.983763

  263. 263.

    Mattman L. Cell Wall Deficient Forms: Stealth Pathogens. 2001.

    Not in our library

  264. 264.

    Mercier R, Kawai Y, Errington J. Excess membrane synthesis drives a primitive mode of cell proliferation. Cell. 2013;152:997-1007.

    Not in our library10.1016/j.cell.2013.01.043

  265. 265.
    General principles for the formation and proliferation of a wall-free (L-form) state in bacteria · 2014
    Not checked
  266. 266.

    Meyer RD. Legionella infections: a review of five years of research. Rev Infect Dis. 1983;5:258-78.

    Not in our library10.1093/clinids/5.2.258

  267. 267.

    Mifkovic A, Skultety J, Pindak D, et al. Specific aspects of acute pancreatitis. Bratisl Lek Listy. 2009;110:544-52.

    Not in our library

  268. 268.

    Mifkovic A, Skultety J, Sykora P, et al. Intra-abdominal hypertension and acute pancreatitis. Bratisl Lek Listy. 2013;114:166-71.

    Not in our library10.4149/bll_2013_036

  269. 269.

    Minasyan H. Erythrocyte and blood antibacterial defense. Eur J Microbiol Immunol. 2014;4:138-43.

    Not in our library10.1556/eujmi.4.2014.2.7

  270. 270.

    Montassier E, Batard E, Gastinne T, et al. Recent changes in bacteremia in patients with cancer: a systematic review of epidemiology and antibiotic resistance. Eur J Clin Microbiol. 2013;32:841-50.

    Not in our library10.1007/s10096-013-1819-7

  271. 271.

    Montes-de-Oca M, Blanco MJ, Marquez M, et al. Haemodynamic derangement in human immunodeficiency virus-infected patients with hepatitis C virus-related cirrhosis: the role of bacterial translocation. Liver Int. 2011;31:850-8.

    Not in our library10.1111/j.1478-3231.2011.02505.x

  272. 272.

    Morgan XC, Huttenhower C. Meta'omic analytic techniques for studying the intestinal microbiome. Gastroenterology. 2014;146:1437-48.

    Not in our library10.1053/j.gastro.2014.01.049

  273. 273.
    Dysfunction of the intestinal microbiome in inflammatory bowel disease and treatment · 2012
    No notice
  274. 274.

    Morita RY. Bacteria in Oligotrophic Environments: Starvation-Survival Lifestyle. 1997.

    Not in our library

  275. 275.

    Muegge BD, Kuczynski J, Knights D, et al. Diet drives convergence in gut microbiome functions across mammalian phylogeny and within humans. Science. 2011;332:970-4.

    Not in our library10.1126/science.1198719

  276. 276.

    Mukamolova GV, Kaprelyants AS, Young DI, et al. A bacterial cytokine. P Natl Acad Sci USA. 1998a;95:8916-21.

    Not in our library10.1073/pnas.95.15.8916

  277. 277.

    Mukamolova GV, Kormer SS, Kell DB, et al. Stimulation of the multiplication of Micrococcus luteus by an autocrine growth factor. Arch Microbiol. 1999;172:9-14.

    Not in our library10.1007/s002030050733

  278. 278.

    Mukamolova GV, Turapov OA, Kazarian K, et al. The rpf gene of Micrococcus luteus encodes an essential secreted growth factor. Mol Microbiol. 2002a;46:611-21.

    Not in our library10.1046/j.1365-2958.2002.03183.x

  279. 279.

    Mukamolova GV, Turapov OA, Young DI, et al. A family of autocrine growth factors in Mycobacterium tuberculosis. Mol Microbiol. 2002b;46:623-35.

    Not in our library10.1046/j.1365-2958.2002.03184.x

  280. 280.

    Mukamolova GV, Yanopolskaya ND, Kell DB, et al. On resuscitation from the dormant state of Micrococcus luteus. Anton Leeuw. 1998b;73:237-43.

    Not in our library10.1023/a:1000881918216

  281. 281.

    Muñoz P, Cruz AF, Rodríguez-Créixems M, et al. Gram-negative bloodstream infections. Int J Antimicrob Ag. 2008;32(Suppl 1):S10-14.

    Not in our library10.1016/j.ijantimicag.2008.06.015

  282. 282.

    Munteanu D, Negru A, Radulescu M, et al. Evaluation of bacterial translocation in patients with chronic HCV infection. Rom J Intern Med. 2014;52:91-6.

    Not in our library

  283. 283.

    Murray PR, Bennett JE, Dolin R, Blaser MJ. The clinician and the microbiology laboratory. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 2015.

    Not in our library

  284. 284.

    Mylotte JM, Tayara A. Blood cultures: clinical aspects and controversies. Eur J Clin Microbiol. 2000;19:157-63.

    Not in our library10.1007/s100960050453

  285. 285.

    Nagalingam NA, Lynch SV. Role of the microbiota in inflammatory bowel diseases. Inflamm Bowel Dis. 2012;18:968-84.

    Not in our library10.1002/ibd.21866

  286. 286.

    Nagata E, de Toledo A, Oho T. Invasion of human aortic endothelial cells by oral viridans group streptococci and induction of inflammatory cytokine production. Mol Oral Microbiol. 2011;26:78-88.

    Not in our library10.1111/j.2041-1014.2010.00597.x

  287. 287.

    Narihiro T, Kamagata Y. Cultivating yet-to-be cultivated microbes: the challenge continues. Microbes Environ. 2013;28:163-5.

    Not in our library10.1264/jsme2.me2802rh

  288. 288.

    Natarajan N, Pluznick JL. From microbe to man: the role of microbial short chain fatty acid metabolites in host cell biology. Am J Physiol-Cell Ph. 2014;307:C979-85.

    Not in our library10.1152/ajpcell.00228.2014

  289. 289.

    Neuman Y. Cryptobiosis: a new theoretical perspective. Prog Biophys Mol Bio. 2006;92:258-67.

    Not in our library10.1016/j.pbiomolbio.2005.11.001

  290. 290.

    Nichols D, Cahoon N, Trakhtenberg EM, et al. Use of ichip for high-throughput in situ cultivation of ‘uncultivable’ microbial species. Appl Environ Microb. 2010;76:2445-50.

    Not in our library10.1128/aem.01754-09

  291. 291.

    Nielsen HH, Qiu J, Friis S, et al. Treatment for Helicobacter pylori infection and risk of Parkinson's disease in Denmark. Eur J Neurol. 2012;19:864-9.

    Not in our library10.1111/j.1468-1331.2011.03643.x

  292. 292.

    Nikkari S, McLaughlin IJ, Bi W, et al. Does blood of healthy subjects contain bacterial ribosomal DNA? J Clin Microbiol. 2001;39:1956-9.

    Not in our library10.1128/jcm.39.5.1956-1959.2001

  293. 293.

    O'Mahony SM, Clarke G, Borre YE, et al. Serotonin, tryptophan metabolism and the brain-gut-microbiome axis. Behav Brain Res. 2015;277:32-48.

    Not in our library10.1016/j.bbr.2014.07.027

  294. 294.

    Ochoa-Repáraz J, Mielcarz DW, Begum-Haque S, et al. Gut, bugs, and brain: role of commensal bacteria in the control of central nervous system disease. Ann Neurol. 2011;69:240-7.

    Not in our library10.1002/ana.22344

  295. 295.

    Ochoa-Repáraz J, Mielcarz DW, Ditrio LE, et al. Role of gut commensal microflora in the development of experimental autoimmune encephalomyelitis. J Immunol. 2009;183:6041-50.

    Not in our library10.4049/jimmunol.0900747

  296. 296.

    Ogrendik M. Efficacy of roxithromycin in adult patients with rheumatoid arthritis who had not received disease-modifying antirheumatic drugs: a 3-month, randomized, double-blind, placebo-controlled trial. Clin Ther. 2009a;31:1754-64.

    Not in our library10.1016/j.clinthera.2009.08.014

  297. 297.

    Ogrendik M. Rheumatoid arthritis is linked to oral bacteria: etiological association. Mod Rheumatol. 2009b;19:453-6.

    Not in our library10.1007/s10165-009-0194-9

  298. 298.

    Ogrendik M. Antibiotics for the treatment of rheumatoid arthritis. Int J Gen Med. 2013a;7:43-7.

    Not in our library10.2147/ijgm.s56957

  299. 299.

    Ogrendik M. Rheumatoid arthritis is an autoimmune disease caused by periodontal pathogens. Int J Gen Med. 2013b;6:383-6.

    Not in our library10.2147/ijgm.s45929

  300. 300.

    Oláh A, Romics L. Enteral nutrition in acute pancreatitis: a review of the current evidence. World J Gastroenterol. 2014;20:16123-31.

    Not in our library10.3748/wjg.v20.i43.16123

  301. 301.

    Owen JL, Mohamadzadeh M. Microbial activation of gut dendritic cells and the control of mucosal immunity. J Interf Cytok Res. 2013;33:619-31.

    Not in our library10.1089/jir.2013.0046

  302. 302.

    Owyang C, Wu GD. The gut microbiome in health and disease. Gastroenterology. 2014;146:1433-6.

    Not in our library10.1053/j.gastro.2014.03.032

  303. 303.

    Page EE, Nelson M, Kelleher P. HIV and hepatitis C coinfection: pathogenesis and microbial translocation. Curr Opin HIV AIDS. 2011;6:472-7.

    Not in our library10.1097/coh.0b013e32834bbc71

  304. 304.

    Pallen MJ, Loman NJ, Penn CW. High-throughput sequencing and clinical microbiology: progress, opportunities and challenges. Curr Opin Microbiol. 2010;13:625-31.

    Not in our library10.1016/j.mib.2010.08.003

  305. 305.

    Parracho HM, Bingham MO, Gibson GR, et al. Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children. J Med Microbiol. 2005;54:987-91.

    Not in our library10.1099/jmm.0.46101-0

  306. 306.

    Percival SL, Hill KE, Williams DW, et al. A review of the scientific evidence for biofilms in wounds. Wound Repair Regen. 2012;20:647-57.

    Not in our library10.1111/j.1524-475x.2012.00836.x

  307. 307.

    Petersen C, Round JL. Defining dysbiosis and its influence on host immunity and disease. Cell Microbiol. 2014;16:1024-33.

    Not in our library10.1111/cmi.12308

  308. 308.
    Exercise induction of gut microbiota modifications in obese, non-obese and hypertensive rats · 2014
    No notice
  309. 309.

    Pflughoeft KJ, Versalovic J. Human microbiome in health and disease. Annu Rev Pathol. 2012;7:99-122.

    Not in our library10.1146/annurev-pathol-011811-132421

  310. 310.

    Pham VH, Kim J. Cultivation of unculturable soil bacteria. Trends Biotechnol. 2012;30:475-84.

    Not in our library10.1016/j.tibtech.2012.05.007

  311. 311.

    Postgate JR. Viability measurements and the survival of microbes under minimum stress. Adv Microb Physiol. 1967;1:1-23.

    Not in our library

  312. 312.

    Postgate JR. Viable counts and viability. Methods Microbiol. 1969;1:611-28.

    Not in our library

  313. 313.

    Postgate JR. Death in Microbes and Macrobes. 1976.

    Not in our library

  314. 314.

    Power SE, O'Toole PW, Stanton C, et al. Intestinal microbiota, diet and health. Brit J Nutr. 2014;111:387-402.

    Not in our library10.1017/s0007114513002560

  315. 315.

    Prajsnar TK, Hamilton R, Garcia-Lara J, et al. A privileged intraphagocyte niche is responsible for disseminated infection of Staphylococcus aureus in a zebrafish model. Cell Microbiol. 2012;14:1600-19.

    Not in our library10.1111/j.1462-5822.2012.01826.x

  316. 316.

    Pretorius E, Bester J, Vermeulen N, et al. Profound morphological changes in the erythrocytes and fibrin networks of patients with hemochromatosis or with hyperferritinemia, and their normalization by iron chelators and other agents. PlosOne. 2014a;9:e85271.

    Not in our library10.1371/journal.pone.0085271

  317. 317.

    Pretorius E, Kell DB. Diagnostic morphology: biophysical indicators for iron-driven inflammatory diseases. Integr Biol. 2014;6:486-510.

    Not in our library10.1039/c4ib00025k

  318. 318.

    Pretorius E, Swanepoel AC, Buys AV, et al. Eryptosis as a marker of Parkinson's disease. Aging. 2014b;6:788-818.

    Not in our library10.18632/aging.100695

  319. 319.

    Pretorius E, Vermeulen N, Bester J, et al. A novel method for assessing the role of iron and its functional chelation in fibrin fibril formation: the use of scanning electron microscopy. Toxicol Mech Method. 2013;23:352-9.

    Not in our library10.3109/15376516.2012.762082

  320. 320.

    Primas H. Chemistry, Quantum Mechanics and Reductionism. 1981.

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  321. 321.

    Proal AD, Albert PJ, Marshall TG, Nelson KE. Autoimmune disease and the human metagenome. Metagenomics of the Human Body. 2011.

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    Proal AD, Albert PJ, Marshall TG, et al. Immunostimulation in the treatment for chronic fatigue syndrome/myalgic encephalomyelitis. Immunol Res. 2013;56:398-412.

    Not in our library10.1007/s12026-013-8413-z

  323. 323.

    Proal AD, Albert PJ, Marshall TG. Inflammatory disease and the human microbiome. Discov Med. 2014;17:257-65.

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  324. 324.
    Evidence for the Gut Microbiota Short-Chain Fatty Acids as Key Pathophysiological Molecules Improving Diabetes · 2014
    No notice
  325. 325.

    Puleo F, Arvanitakis M, Van Gossum A, et al. Gut failure in the ICU. Semin Respir Crit Care. 2011;32:626-38.

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    Puspita DI, Kamagata Y, Tanaka M, et al. Are uncultivated bacteria really uncultivable? Microbes Environ. 2012;27:356-66.

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    Puspita DI, Uehara M, Katayama T, et al. Resuscitation promoting factor (Rpf) from Tomitella biformata AHU 1821(T) promotes growth and resuscitates non-dividing cells. Microbes Environ. 2013;28:58-64.

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  328. 328.

    Qin J, Li Y, Cai Z, et al. A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature. 2012;490:55-60.

    Not in our library10.1038/nature11450

  329. 329.

    Radajewski S, Ineson P, Parekh NR, et al. Stable-isotope probing as a tool in microbial ecology. Nature. 2000;403:646-9.

    Not in our library10.1038/35001054

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    Ramírez JH, Parra B, Gutierrez S, et al. Biomarkers of cardiovascular disease are increased in untreated chronic periodontitis: a case control study. Aust Dent J. 2014;59:29-36.

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  332. 332.

    Rechner AR, Kuhnle G, Hu H, et al. The metabolism of dietary polyphenols and the relevance to circulating levels of conjugated metabolites. Free Radical Res. 2002;36:1229-41.

    Not in our library10.1080/246-1071576021000016472

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    Renesto P, Crapoulet N, Ogata H, et al. Genome-based design of a cell-free culture medium for Tropheryma whipplei. Lancet. 2003;362:447-9.

    Not in our library10.1016/s0140-6736(03)14071-8

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    Renko J, Lepp PW, Oksala N, et al. Bacterial signatures in atherosclerotic lesions represent human commensals and pathogens. Atherosclerosis. 2008;201:192-7.

    Not in our library10.1016/j.atherosclerosis.2008.01.006

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    Rhee SH. Lipopolysaccharide: basic biochemistry, intracellular signaling, and physiological impacts in the gut. Intest Res. 2014;12:90-5.

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    Rinke C, Schwientek P, Sczyrba A, et al. Insights into the phylogeny and coding potential of microbial dark matter. Nature. 2013;499:431-7.

    Not in our library10.1038/nature12352

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    Robles-Alonso V, Guarner F. From basic to applied research: lessons from the human microbiome projects. J Clin Gastroenterol. 2014;48(Suppl 1):S3-4.

    Not in our library10.1097/mcg.0000000000000242

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  339. 339.

    Rolain JM, Maurin M, Mallet MN, et al. Culture and antibiotic susceptibility of Bartonella quintana in human erythrocytes. Antimicrob Agents Ch. 2003;47:614-9.

    Not in our library10.1128/aac.47.2.614-619.2003

  340. 340.

    Ronco C. Endotoxin removal: history of a mission. Blood Purif. 2014;37(Suppl 1):5-8.

    Not in our library10.1159/000356831

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    Rooks MG, Veiga P, Wardwell-Scott LH, et al. Gut microbiome composition and function in experimental colitis during active disease and treatment-induced remission. ISME J. 2014;8:1403-17.

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  342. 342.

    Rosenfeld ME, Campbell LA. Pathogens and atherosclerosis: update on the potential contribution of multiple infectious organisms to the pathogenesis of atherosclerosis. Thromb Haemostasis. 2011;106:858-67.

    Not in our library10.1160/th11-06-0392

  343. 343.

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    Not in our library10.1093/ndt/gfu287

  345. 345.

    Sacchi P, Cima S, Corbella M, et al. Liver fibrosis, microbial translocation and immune activation markers in HIV and HCV infections and in HIV/HCV co-infection. Dig Liver Dis. 2015;47:218-25.

    Not in our library10.1016/j.dld.2014.11.012

  346. 346.

    Sahin N, Gonzalez JM, Iizuka T, et al. Characterization of two aerobic ultramicrobacteria isolated from urban soil and a description of Oxalicibacterium solurbis sp. nov. FEMS Microbiol Lett. 2010;307:25-9.

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  347. 347.

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  348. 348.

    Salipante SJ, Roach DJ, Kitzman JO, et al. Large-scale genomic sequencing of extraintestinal pathogenic Escherichia coli strains. Genome Res. 2015;25:119-28.

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  349. 349.
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    No notice
  350. 350.
    Reagent and laboratory contamination can critically impact sequence-based microbiome analyses · 2014
    No notice
  351. 351.

    Sánchez-Calvo JM, García-Castillo M, Lamas A, et al. Gut microbiota composition in cystic fibrosis patients: molecular approach and classical culture. J Cyst Fibros. 2008;7:S50.

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    Sandler NG, Douek DC. Microbial translocation in HIV infection: causes, consequences and treatment opportunities. Nat Rev Microbiol. 2012;10:655-66.

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    Sanz Y, Moya-Pérez A. Microbiota, inflammation and obesity. Adv Exp Med Biol. 2014;817:291-317.

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    Sato J, Kanazawa A, Ikeda F, et al. Gut dysbiosis and detection of ‘live gut bacteria’ in blood of Japanese patients with type 2 diabetes. Diabetes Care. 2014;37:2343-50.

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    Sato S, Kiyono H, Fujihashi K. Mucosal immunosenescence in the gastrointestinal tract: a mini-review. Gerontology. 2014.

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  357. 357.

    Sayin SI, Wahlstrom A, Felin J, et al. Gut microbiota regulates bile acid metabolism by reducing the levels of tauro-beta-muricholic acid, a naturally occurring FXR antagonist. Cell Metab. 2013;17:225-35.

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  358. 358.

    Scanlan PD, Buckling A, Kong W, et al. Gut dysbiosis in cystic fibrosis. J Cyst Fibros. 2012;11:454-5.

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    Scher JU, Abramson SB. The microbiome and rheumatoid arthritis. Nat Rev Rheumatol. 2011;7:569-78.

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  367. 367.

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    Sharma BR. Infection in patients with severe burns: causes and prevention thereof. Infect Dis Clin N Am. 2007;21:745-59.

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    Shaw MK. Cell invasion by Theileria sporozoites. Trends Parasitol. 2003;19:2-6.

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    Tanaka T, Kawasaki K, Daimon S, et al. A hidden pitfall in the preparation of agar media undermines microorganism cultivability. Appl Environ Microb. 2014;80:7659-66.

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  385. 385.
    The Integrative Human Microbiome Project: Dynamic Analysis of Microbiome-Host Omics Profiles during Periods of Human Health and Disease · 2014
    No notice
  386. 386.

    Thwaites GE, Gant V. Are bloodstream leukocytes Trojan Horses for the metastasis of Staphylococcus aureus? Nat Rev Microbiol. 2011;9:215-22.

    Not in our library10.1038/nrmicro2508

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    Tomas-Barberan F, Garcia-Villalba R, Quartieri A, et al. In vitro transformation of chlorogenic acid by human gut microbiota. Mol Nutr Food Res. 2014;58:1122-31.

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    Not in our library10.1038/nature05414

  394. 394.

    Vaarala O. Human intestinal microbiota and type 1 diabetes. Curr Diabetes Rep. 2013;13:601-7.

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  395. 395.

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    Not in our library10.1038/mi.2014.107

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    Venkatesh M, Mukherjee S, Wang H, et al. Symbiotic bacterial metabolites regulate gastrointestinal barrier function via the xenobiotic sensor PXR and Toll-like receptor 4. Immunity. 2014;41:296-310.

    Not in our library10.1016/j.immuni.2014.06.014

  403. 403.

    Vila-Corcoles A, Ochoa-Gondar O, Rodriguez-Blanco T, et al. Evaluating clinical effectiveness of pneumococcal vaccination in preventing stroke: the CAPAMIS Study 3-year follow-up. J Stroke Cerebrovasc. 2014;23:1577-84.

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  404. 404.

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    Not in our library10.1001/jama.2009.1754

  405. 405.

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    Not in our library10.1128/iai.01779-14

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    Vizcarra JA, Wilson-Perez HE, Espay AJ. The power in numbers: gut microbiota in Parkinson's disease. Movement Disord. 2015;30:296-8.

    Not in our library10.1002/mds.26116

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    Vogl G, Plaickner A, Szathmary S, et al. Mycoplasma gallisepticum invades chicken erythrocytes during infection. Infect Immun. 2008;76:71-7.

    Not in our library10.1128/iai.00871-07

  408. 408.

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    Not in our library10.1128/aem.60.9.3284-3291.1994

  409. 409.

    Vujkovic-Cvijin I, Dunham RM, Iwai S, et al. Dysbiosis of the gut microbiota is associated with HIV disease progression and tryptophan catabolism. Sci Transl Med. 2013;5:193-1.

    Not in our library10.1126/scitranslmed.3006438

  410. 410.

    Walker AW, Duncan SH, Louis P, et al. Phylogeny, culturing, and metagenomics of the human gut microbiota. Trends Microbiol. 2014;22:267-74.

    Not in our library10.1016/j.tim.2014.03.001

  411. 411.

    Wallet F, Loiez C, Herwegh S, et al. Usefulness of real-time PCR for the diagnosis of sepsis in ICU-acquired infections. Infect Disord Drug Targets. 2011;11:348-53.

    Not in our library10.2174/187152611796504845

  412. 412.

    Wang Y, Chen Y, Zhou Q, et al. A culture-independent approach to unravel uncultured bacteria and functional genes in a complex microbial community. PLoS One. 2012c;7:e47530.

    Not in our library10.1371/journal.pone.0047530

  413. 413.

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    Not in our library10.1038/nature09922

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    Not in our library10.1371/journal.pone.0050314

  415. 415.

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    Not in our library10.1007/s00415-012-6558-7

  416. 416.

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    Not in our library10.1038/nature11553

  418. 418.

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    Not in our library10.1098/rspb.2002.2209

  419. 419.

    Wiest R, Garcia-Tsao G. Bacterial translocation (BT) in cirrhosis. Hepatology. 2005;41:422-33.

    Not in our library10.1002/hep.20632

  420. 420.

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    Not in our library10.1016/j.jhep.2013.07.044

  421. 421.

    Wiest R, Rath HC. Gastrointestinal disorders of the critically ill. Bacterial translocation in the gut. Best Pract Res Cl Ga. 2003;17:397-425.

    Not in our library10.1016/s1521-6918(03)00024-6

  422. 422.

    Wikoff WR, Anfora AT, Liu J, et al. Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. P Natl Acad Sci USA. 2009;106:3698-703.

    Not in our library10.1073/pnas.0812874106

  423. 423.

    Williams BB, Van Benschoten AH, Cimermancic P, et al. Discovery and characterization of gut microbiota decarboxylases that can produce the neurotransmitter tryptamine. Cell Host Microbe. 2014;16:495-503.

    Not in our library10.1016/j.chom.2014.09.001

  424. 424.
    Impaired Carbohydrate Digestion and Transport and Mucosal Dysbiosis in the Intestines of Children with Autism and Gastrointestinal Disturbances · 2011
    No notice
  425. 425.

    Williams BL, Hornig M, Parekh T, et al. Application of novel PCR-based methods for detection, quantitation, and phylogenetic characterization of Sutterella species in intestinal biopsy samples from children with autism and gastrointestinal disturbances. MBio. 2012;3:00261–11.

    Not in our library10.1128/mbio.00261-11

  426. 426.

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    Not in our library10.1038/nature12779

  427. 427.

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    Not in our library

  428. 428.

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    Not in our library10.1038/nature09415

  429. 429.

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    Not in our library10.1073/pnas.74.11.5088

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    Not in our library10.1073/pnas.87.12.4576

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    Xayarath B, Freitag NE. Optimizing the balance between host and environmental survival skills: lessons learned from Listeria monocytogenes. Future Microbiol. 2012;7:839-52.

    Not in our library10.2217/fmb.12.57

  432. 432.
    Streptococcus pneumoniae invades erythrocytes and utilizes them to evade human innate immunity. · 2013
    Not checked
  433. 433.

    Yang J, Feng L, Ren J, et al. Correlation between the severity of periodontitis and coronary artery stenosis in a Chinese population. Aust Dent J. 2013;58:333-8.

    Not in our library10.1111/adj.12087

  434. 434.

    Yarza P, Spröer C, Swiderski J, et al. Sequencing orphan species initiative (SOS): filling the gaps in the 16S rRNA gene sequence database for all species with validly published names. Syst Appl Microbiol. 2013;36:69-73.

    Not in our library10.1016/j.syapm.2012.12.006

  435. 435.

    Yatsunenko T, Rey FE, Manary MJ, et al. Human gut microbiome viewed across age and geography. Nature. 2012;486:222-7.

    Not in our library10.1038/nature11053

  436. 436.

    Young D, Stark J, Kirschner D. Systems biology of persistent infection: tuberculosis as a case study. Nat Rev Microbiol. 2008;6:520-8.

    Not in our library10.1038/nrmicro1919

  437. 437.

    Yu RQ, Yuan JL, Ma LY, et al. Probiotics improve obesity-associated dyslipidemia and insulin resistance in high-fat diet-fed rats. Zhongguo Dang Dai Er Ke Za Zhi. 2013;15:1123-7.

    Not in our library

  438. 438.

    Zengler K, Toledo G, Rappe M, et al. Cultivating the uncultured. P Natl Acad Sci USA. 2002;99:15681-6.

    Not in our library10.1073/pnas.252630999

  439. 439.

    Zhang H, Liao X, Sparks JB, et al. Dynamics of gut microbiota in autoimmune lupus. Appl Environ Microb. 2014a;80:7551-60.

    Not in our library10.1128/aem.02676-14

  440. 440.

    Zhang R, Lahens NF, Ballance HI, et al. A circadian gene expression atlas in mammals: implications for biology and medicine. P Natl Acad Sci USA. 2014b;111:16219-24.

    Not in our library10.1073/pnas.1408886111

  441. 441.

    Zhang Y, Yew WW, Barer MR. Targeting persisters for tuberculosis control. Antimicrob Agents Ch. 2012;56:2223-30.

    Not in our library10.1128/aac.06288-11

  442. 442.

    Zhang Y, Zou Y, Ma P, et al. Identification of Mycoplasma suis MSG1 interaction proteins on porcine erythrocytes. Arch Microbiol. 2014c;80:7551-60.

    Not in our library10.1007/s00203-014-1050-7

  443. 443.

    Zhu Y, Jameson E, Crosatti M, et al. Carnitine metabolism to trimethylamine by an unusual Rieske-type oxygenase from human microbiota. P Natl Acad Sci USA. 2014;111:4268-73.

    Not in our library10.1073/pnas.1316569111

  444. 444.

    Zimmermann MB, Chassard C, Rohner F, et al. The effects of iron fortification on the gut microbiota in African children: a randomized controlled trial in Cote d'Ivoire. Am J Clin Nutr. 2010;92:1406-15.

    Not in our library10.3945/ajcn.110.004564

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