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Systematic Review: The Gut Microbiome and Its Potential Clinical Application in Inflammatory Bowel Disease

Laila Aldars-García, María Chaparro, Javier P. Gisbert

Microorganisms · 2021 · Review · CC BY

doi:10.3390/microorganisms9050977

Abstract

Inflammatory bowel disease (IBD) is a chronic relapsing–remitting systemic disease of the gastrointestinal tract. It is well established that the gut microbiome has a profound impact on IBD pathogenesis. Our aim was to systematically review the literature on the IBD gut microbiome and its usefulness to provide microbiome-based biomarkers. A systematic search of the online bibliographic database PubMed from inception to August 2020 with screening in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was conducted. One-hundred and forty-four papers were eligible for inclusion. There was a wide heterogeneity in microbiome analysis methods or experimental design. The IBD intestinal microbiome was generally characterized by reduced species richness and diversity, and lower temporal stability, while changes in the gut microbiome seemed to play a pivotal role in determining the onset of IBD. Multiple studies have identified certain microbial taxa that are enriched or depleted in IBD, including bacteria, fungi, viruses, and archaea. The two main features in this sense are the decrease in beneficial bacteria and the increase in pathogenic bacteria. Significant differences were also present between remission and relapse IBD status. Shifts in gut microbial community composition and abundance have proven to be valuable as diagnostic biomarkers. The gut microbiome plays a major role in IBD, yet studies need to go from casualty to causality. Longitudinal designs including newly diagnosed treatment-naïve patients are needed to provide insights into the role of microbes in the onset of intestinal inflammation. A better understanding of the human gut microbiome could provide innovative targets for diagnosis, prognosis, treatment and even cure of this relevant disease.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 23, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

The gastrointestinal microbiota comprises a collection of microbial communities, including viruses, bacteria, archaea and fungi, inhabiting the gastrointestinal tract. The constitution and diversity of the microbiota in different sections of the gastrointestinal tract are highly variable and its concentration increases steadily along it, with small numbers in the stomach and very high concentrations in the colon. This community has been linked to many diseases, including inflammatory bowel disease (IBD).

IBD encompasses a group of chronic inflammatory bowel pathologies of idiopathic origin that affect millions of people throughout the world; the two most important pathologies covered by this term are Crohn’s disease (CD) and ulcerative colitis (UC). IBD is not curable and shows a chronic evolution, with alternating periods of exacerbation and remission. This situation entails a high burden on health care systems, which try to provide treatment and to ensure quality of life for these complex patients who often require lifelong medical attention.

The microbiota of the gastrointestinal tract is frequently proposed as one of the key players in the etiopathogenesis of IBD. Studies in animal models and humans have shown that there is a persistent imbalance of the intestinal microbiome (which refers to the gut microbiota and their collective genetic material) related to IBD, with a substantial body of literature providing evidence for the relation of the human gut microbiome and IBD. Despite all this evidence, it has been difficult to determine whether these changes in the microbiome are the cause of IBD or rather the result of inflammation after IBD onset. The consequence of this relationship between the human gut and microbes is that pharmacological therapies, diet and other interventions targeted to the host will also significantly impact the gut microbiota. Most of the existing studies attempting to determine whether dysbiosis is causative or a consequence of inflammation had certain limitations, such as disparities in methodologic approaches, including different techniques used to analyze the gut microbiome, different sampling sites (stool/mucosa) or site of inflammation, lack of prospective data, small cohort sizes, restricted focus on bacteria, different disease activities and influence of treatment interventions.

We conducted a systematic review to comprehensively collate the body of evidence surrounding the relationship between the gut microbiome and IBD. Our objective was to describe the associations between IBD and dysbiosis and the potential clinical translation of microbiome-based biomarkers.

2.1. Search Strategy

An electronic search was conducted using the MEDLINE database via PubMed to identify published articles on the gut microbiome and IBD, from inception to August 2020. The search strings used were:

[(“ulcerative colitis” [MeSH Terms]) OR (“colitis” [All Fields] AND “ulcerative” [All Fields]) OR (“ulcerative colitis” [All Fields]) OR (“crohn disease” [MeSH Terms]) OR (“crohn” [All Fields] AND “disease” [All Fields]) OR (“crohn disease” [All Fields]) OR (“crohn’s disease” [All Fields]) OR (“inflammatory bowel diseases” [MeSH Terms]) OR (“inflammatory bowel diseases” [All Fields])] AND (“microbiome” [All Fields] OR “microbiota” [All Fields]).

Moreover, the reference lists of the included studies were revised to identify further relevant studies.

The work was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement in Appendix A.

2.2. Eligibility Criteria

The inclusion criteria were intestinal microbiome studies comparing IBD patients with controls; performed on fecal, intestinal lavage or intestinal tissue samples; focused on human adults; written in English.

Studies were excluded if they reported data on IBD complications or postsurgery (pouchitis, fistulae, among others); studied other conditions in addition to IBD (irritable bowel syndrome, Clostridium difficile infection, primary sclerosing cholangitis, among others); were abstracts from conference proceedings, letters to editor, reviews or reported only one patient.

3. Results

A total of 5267 records were identified from the PUBMED database. Of 190 papers remaining after screening, 23 did not include controls, 22 included other pathologies and 2 were in silico studies. A total of 143 papers were ultimately included.

3.1. Gut Microbiome Studies in IBD: Methodologic Aspects

The main methodologic characteristics of the studies included in this review are summarized in Table 1 (IBD gut microbiome studies using non-next-generation sequencing [NGS] approaches) and Table 2 (IBD gut microbiome studies using NGS approaches).

3.1.1. Study Design

Across the included studies, populations ranged from 2 to 531 patients, many of them with a small sample size that reduced the precision of the estimations. Thus, since many results are limited by sample size, further studies with larger cohorts are desirable to confirm these results and to clarify the significance of the microbiome in the pathogenesis of IBD.

In addition, to date, most published studies in IBD are cross-sectional (121 out of the 143 reviewed studies). However, longitudinal designs are required to capture changes that precede or coincide with disease and symptom onset, and to mechanistically relate microbiome shifts with disease pathogenesis. Overall, longitudinal studies in IBD (only 15% of the included studies) indicate that there is decreased stability in the microbiota composition in UC and CD patients. These dynamic changes emphasize the importance of longitudinal sampling for a better understanding of taxa stability in individuals.

The IBD microbiome varies not only over time but also with treatment. Newly diagnosed patients with no treatment provide an ideal scenario to study the potential etiopathogenesis related to intestinal dysbiosis that occurs in IBD. Mouse and human studies have proven that the gut microbiome is required for disease onset, as germ-free mice rarely develop the disease, antibiotics can prevent disease onset in mice and ameliorate (but not cure) the disease in humans.

However, prior IBD microbiome studies have mostly included subjects with an established treatment; of the 143 microbiome studies included herein, only 11 included treatment-naïve patients, sometimes only on a small subset of the cohort, and only one was conducted prospectively.

Results on newly diagnosed treatment-naïve patients showed that gut dysbiosis is already established at the beginning of the disease. The dysbiotic profile in the gut of newly diagnosed treatment-naïve IBD patients presents reduced microbial abundance, less biodiversity in the structure of microbial communities, and differential bacterial abundances compared to the profile of established and treated IBD patients or control groups. Conversely, one study showed none or minor microbial differences between these patients and a control group.

Current knowledge, despite some controversy, provides valuable insights supporting the idea that microbial alterations may precede IBD onset. Given the limited number of studies in this type of patients, no consistent conclusion can be inferred, and further work is needed to investigate in depth the gut dysbiosis of newly diagnosed treatment-naïve IBD patients.

3.1.2. Microbiome Analysis Methods

Culture-independent and -dependent methods for microbial community analysis have both been used to describe microorganisms from different environments, including the human gut. However, due to the inability to culture the majority of the resident bacteria from the gastrointestinal tract, culture-independent methods have proven much more reliable and faster in profiling complex microbial communities.

Culture-independent techniques are based on sequence divergences of the small subunit ribosomal RNA (16S rRNA) or other target gene regions. Some of these techniques are quantitative real-time PCR (qPCR), denaturing gradient gel electrophoresis (DGGE), terminal restriction fragment length polymorphism (T-RFLP), fluorescence in situ hybridization (FISH), DNA microarrays, and NGS. All these techniques, except for NGS, are referred herein as non-NGS techniques.

Currently, there are many differences in study design and methodology among studies, making translation of basic science results into clinical practice a challenging task. Among the studies included in this review, very few used culture-dependent techniques (7 out of 143); and over the years, NGS became the most employed technique—79 studies used NGS, while 64 studies used non-NGS approaches.

Lately, the most widely used approaches are amplicon gene sequencing, predominantly the 16S rRNA gene (16S rDNA), and whole-genome shotgun sequencing, both NGS techniques.

Another recent technique much less used in this field is flow cytometry. A recent study demonstrated that cytometry fingerprints can be used as a diagnostic tool to classify samples according to CD state. These results highlight the potential of flow cytometry as a tool to conduct rapid and cheaper diagnostics of microbiome-associated diseases.

3.1.3. Sample Type and Site

Currently, bacterial diversity in the human gut is determined through analysis of the luminal content (stool) and mucosal biopsies; however, the stool microbiome differs from the mucosa-associated microbiome. Most of the bacteria are tightly adhered to the mucus and this mucosa-adhered microbiota may be associated with the pathogenesis of the disease. Changes observed in stool samples likely represent an indirect measure of what is happening at the mucosal surface, where microorganisms interact more intimately with the host and induce disease.

The studies reviewed herein used fecal data, biopsy data or both, and most of them showed differences between fecal and biopsy samples, although a few studies found similarities. The reported differences in microbial composition related to whether the sample origin was fecal or mucosal indicate that each biological sample represents a different environment thus emphasizing the importance of experimental design. Biopsies are primarily recommended for the dissection of the complex pathogenesis of IBD, whereas feces could effectively detect key biomarkers, enabling non-invasive continuous disease monitoring.

In biopsy samples, sampling site can also be a confounding factor. Many studies have compared the microbiome of inflamed and non-inflamed tissue from the same IBD patient. Regarding the effect of gut inflammation on the microbiota, there are some discrepancies among studies. Some researchers did not find significant differences in the mucosa-associated bacteria between apparently normal and inflamed mucosa in IBD patients. Conversely, other studies found gut microbiome differences between inflamed and non-inflamed regions in mucosal biopsies. This difference was also observed in fungal communities of inflamed mucosa, which are distinguishable from those of the non-inflamed area.

In spite of the controversial results, there is evidence supporting that inflamed and non-inflamed tissue samples in both CD and UC may present some differential microbiota composition suggesting that a comparison of mucosal samples obtained from identical sites in IBD patients and non-IBD controls is needed to avoid the confounding effect of inflammation in the assessment of the microbial profile.

3.1.4. Structural and Functional Analysis

IBD microbiome studies have typically focused on characterizing the composition of a community and less attention has been paid to functional profiles of the microbes within a community. Functional information can be inferred from the taxa through bioinformatic approaches or directly assessed via whole-genome shotgun sequencing.

Function is more informative than taxonomy as it provides information on possible mechanisms acting on microbes and on microbe–host interactions, which are important for understanding microbial communities, specially microbiome-related diseases. The loss of a particular function could be more biologically meaningful than the loss of a single or a group of species.

The vast majority of the studies published on the IBD microbiome to date have focused on taxonomy and the reported associations in the IBD gut microbiome are largely limited to identifying high-level taxonomic classification (ranging from phyla to genera) given, for example, the limitations of amplicon gene sequencing for reliable species identification.

Some IBD gut microbiome studies have assessed the change in microbial function compared to healthy subjects. Outcomes of such studies showed a quite distinct change in microbial functions, such as fecal tryptic activity, oxidative response or lipid and glycan metabolism pathways. Based on these results, it is necessary to redirect the study of dysbiosis from a purely compositional definition to a definition that includes functional changes of the microbiota.

3.2. Dysbiosis in IBD

The microbiome is different among healthy individuals around the globe, and the great differences found between the microbiomes of apparently healthy people complicate the definition of a healthy microbiome. Despite this divergence, the vast and diverse microbial gut community lives in relative balance in healthy individuals. Dysbiosis refers to an imbalance in microbial species, which is commonly associated with impaired gut barrier function and inflammatory activity. It encompasses major traits such as loss of beneficial microbes, expansion of pathobionts, and loss of diversity (Figure 1). The following sections will describe the key alterations found in the gut of IBD patients.

3.2.1. Defining the Gut Microbiome in IBD

Although the gastrointestinal tract contains trillions of resident microorganisms that include bacteria, archaea, fungi and viruses, the studies revised herein highlighted that current research on microbiome is mainly focused on bacteria.

Bacterial Dysbiosis

It has consistently been shown that there is a disease-dependent restriction of biodiversity and an imbalanced bacterial composition associated with IBD. The abundance of beneficial microorganisms such as Clostridium groups IV and XIVa, Bacteroides, Suterella, Roseburia, Bifidobacterium species and Faecalibacterium prausnitzii is reduced, whereas some pathogens such as Proteobacteria members (including invasive and adherent Escherichia coli), Veillonellaceae, Pasteurellaceae, Fusobacterium species, and Ruminococcus gnavus are increased. Most of the studies have revealed that in IBD patients, commensal bacteria are depleted and the microbial community is less diverse.

The increase in the phylum Proteobacteria, which includes multiple genera considered potentially pathogenic such as Escherichia, Salmonella, Yersinia, Desulfovibrio, Helicobacter or Vibrio, has been extensively reported in IBD patients.

In the Firmicutes phylum, F. prausnitzii, an anti-inflammatory commensal bacterium, is frequently decreased in CD, while less evidence has been reported in UC, where it is sometimes increased and in other studies decreased. Specific decrease in Roseburia spp. in patients with IBD has also been consistently noted. Both bacteria are known to be involved in the production of butyrate, an important energy source for intestinal epithelial cells, which strengthens gut barrier function and exerts important immunomodulatory functions. In this same phylum, the mucin degrader R. gnavus is frequently increased in IBD patients’ gut, which may impair barrier stability and contribute to inflammation.

Fungal Dysbiosis

Despite the large body of literature on the IBD gut bacterial microbiome, little has been published on the gut mycobiome; specifically, only nine studies reviewed herein included fungal analysis.

Fungi are ubiquitous and their presence in the gastrointestinal tract has been demonstrated. It was already evidenced many years ago that antibodies directed against mannoproteins of Saccharomyces cerevisiae (ASCA) were associated with CD, suggesting an inappropriate immune response to fungi in these patients.

Although fungi only constitute approximately 0.1% of the total microbial community in the gut, changes in gut mycobiota have been reported in IBD patients. However, results on fungal diversity are controversial; compared to controls, some studies have shown that fungal diversity is decreased in UC patients, and in CD, diversity and richness have been reported to be either increased, reduced, or unchanged. Findings across fungal studies have consistently shown an increase in fungal load, especially in Candida albicans.

Nowadays, the exact mechanisms of intestinal fungi in IBD remain unclear and microbiome studies need to include fungi to properly address the complex challenges of this promising field.

Viral Dysbiosis

The human gut virome includes a diverse collection of viruses, mostly bacteriophages, directly impacting on human health. In this systematic review, only seven studies included viral analysis. Alterations in IBD gut virome showed an expansion of Caudovirales and an inverse correlation between the virome and bacterial microbiome, suggesting an hypothesis where changes in the gut virome may affect bacterial dysbiosis. The use of data on both bacteriome and virome composition would contribute to improve classification between health and disease.

These findings suggest that the loss of virus-bacterium relationships can cause microbiota dysbiosis and intestinal inflammation. However, whether viruses have a direct role in IBD pathogenesis, or merely reflect underlying dysbiosis remains to be determined.

Archaeal Dysbiosis

The human gut microbiota also contains prokaryotes of the domain Archaea. Methane-producing archaea (methanogens) have been associated with disorders of the gastrointestinal tract and dysbiosis. Methanogens play an important role in digestion, improving polysaccharide fermentation by preventing accumulation of acids, reaction end-products and hydrogen gas.

The two reviewed studies including archaeal analysis have shown that the variable prevalence of methanogens in different individuals may play an important role on IBD pathogenesis. Lecours et al. showed that the abundance of Methanosphaera stastmanae in fecal samples was significantly higher in IBD patients than in healthy subjects. Interestingly, only IBD patients developed a significant anti-Msp. stadtmanae immunoglobulin G response, indicating that the composition of archaeal microbiome appears to be an important determinant of the presence or absence of autoimmunity.

The other study demonstrated an inverse association between Methanobrevibacter smithii load and susceptibility to IBD, which could be extended to IBD patients in remission as they found that Mbb. smithii load was markedly higher in healthy subjects compared to IBD patients.

Although archaeal diversity in the gastrointestinal tract is far lower than that of bacteria, these microorganisms can also exert inflammatory effects and their consideration in microbiome studies may be crucial for developing optimal diagnostics and prognostics tools.

Disease Activity and Severity

Different disease activity and severity have been described among IBD patients with a given clinically defined condition, suggesting that, in the context of microbiome dysfunction, each condition may present different microbial profiles. The reviewed studies showed a clear difference in the gut microbiota associated with different disease activity and severity in IBD patients.

Dysbiosis was evidenced by Tong et al. at remission, where highly preserved microbial groups accurately classified IBD status during disease quiescence, suggesting that microbial dysbiosis in IBD may be an underlying disorder not only associated with active disease. In general, compared to inactive disease, bacterial diversity and richness are reduced in active disease. Studies of intestinal microbiota in active/inactive IBD patients have consistently shown an increase in F. prausnitzii and Clostridiales in inactive IBD compared to active IBD, and the increase in Proteobacteria in active IBD compared to inactive IBD. Besides, F. prausnitzii and R. hominis display an inverse correlation with disease activity.

Some studies showed that the genus Bifidobacterium is significantly decreased in stool samples during the active phase of CD and UC compared to the remission phase. On the contrary, biopsies showed a higher abundance of Bifidobacterium during active UC, and the proportion of Bifidobacterium was significantly higher in biopsies than in the fecal samples in active CD patients. Some controversial results were also found as other researchers did not find a correlation between microbiota and disease actitivity.

Regarding IBD severity, different microbial abundance was detected in both biopsies and fecal samples from patients with more aggressive disease, and gut dysbiosis was not only related to current activity but also to the course of the disease. In biopsies, Firmicutes showed a significant decrease and Proteobacteria a significant increase in more aggressive CD, and Bifidobacterium was inversely correlated with IBD severity. The risk of flare was associated with reduced microbial richness, increased dysbiosis index and higher individualized microbial instability.

This area is still in its infancy and some results are inconsistent between studies. Several studies have evidenced microbiota signatures of disease activity and severity and the likelihood of a flare-up. However, more research is necessary to identify specific microbial taxa.

3.3. Gut Microbiome-Based Biomarkers in IBD

Ideal biomarkers should be easy to obtain, easy to determine, non-invasive, cheap, and capable of providing rapid and reproducible results. Non-invasive tests for IBD are already available, including serum antibodies, imaging-based screenings, and fecal biomarkers. However, endoscopy remains the gold standard for IBD diagnosis, as the aforementioned non-invasive tests are limited to active disease and their outcome can be interfered by diseases other than IBD limiting their clinical utility.

As a non-invasive, cost-effective technique, microbiome-based biomarkers might have great potential for early-stage disease detection and disease course prognosis as well as for treatment based on patient stratification. To this end, several attempts have been made to develop indices of dysbiosis based on relative abundances of selected microbial taxa in IBD patients compared to those of a healthy population. In stool samples, a machine learning algorithm using a combination of 50 operational taxonomic units was able to differentiate remission from active CD, and the genera Collinsella and Methanobrevibacter could be used to differentiate between UC and CD. In biopsies, Faecalibacteria and Papillibacter were indicators of IBD status, F. prausnitzii and E. coli were used for differential diagnosis of CD (ileal/colonic), supervised learning classification models were able to classify IBD at specific intestinal locations, and microbiome shifts predicted patient outcome. In biopsies, stool and blood a dysbiosis score accurately stratified IBD patients.

In the previous sections, differential results on the gut microbiome between CD and UC, IBD and healthy subjects or between different disease activities have been described. Such research on the IBD microbiome has evidenced that (1) alterations in the abundance of certain microbial taxa or (2) in the structure of the microbial community, (3) the decreased bacterial richness and/or diversity and (4) the decreased microbial community stability could be used as potential biomarkers in the field.

Nevertheless, due to the high microbiome diversity between individuals, and within the same individual over time, the predictive value of these potential indicators is currently far below the level required for utility in diagnosis, prognosis, or response to treatment. Nonetheless, the increasing number of microbiome studies along with the use of longitudinal approaches pave the way to the refinement of microbiome-based biomarkers as useful disease indicators.

4. Concluding Remarks and Future Perspectives

The study of the human microbiome and its involvement in human health is nowadays one of the most active research topics in biomedicine. A simple search for “Microbiota” and “disease” within PubMed Database reveals almost 28,000 hits to date (august 2020). Given the potential clinical application of the microbiome, the number of studies in this field is rapidly increasing. However, some limitations can be found across these studies, including different methodologic approaches, small cohort sizes, different microbiome analysis methods and sample types and sites, main focus on bacteria, and influence of disease activity and treatment interventions. Therefore, these limitations result in variable findings, difficulty to establish comparison between studies and lack of reproducibility of microbiome signatures across studies.

Recent studies based on novel DNA sequencing methods have revealed major differences in microbial taxonomic and functional composition between IBD patients and healthy individuals. The current knowledge guides us to move our focus from community composition to the understanding of the interactions between microbial functions and the IBD gut microbiome.

The microbiota is very specific to an individual and variable in time, and therefore studies need to go from searching for correlation to searching for causation through longitudinal approaches. One important factor that we must keep in mind when studying the microbiome is that it is a “living entity” subject to variability. This variability is even more evident in the IBD microbiome. To better understand the IBD–microbiome connection, we require prospective longitudinal studies, along with following populations with early-onset IBD. The question of whether dysbiosis precedes the development of IBD and sets the inflammatory process, or merely reflects the altered immune and metabolic environment of the inflamed mucosa, remains to be answered. For this reason, it is of paramount importance to study newly diagnosed treatment-naïve patients, where the microbiome can be studied at the beginning of the disease and without the influence of any IBD treatment. Developing unified approaches to the accurate quantitative assessment of the gut microbiome would contribute to comparisons among studies and to its further clinical application.

The main feature in IBD gut dysbiosis is the decrease in beneficial bacteria and the increase in pathogens. Gut microbiome studies are mainly focused on bacteria, yet beyond bacteria, the gut microbiome is composed of other microorganisms such as viruses, fungi or archaea, which play a role in IBD etiology and/or in bacterial population control. In addition, it is currently known that disease activity and severity influence the gut microbiome, thereby affecting the results. IBD can be considered as a “multimicrobial” disease with no single causative microorganism, in which more severe disease is linked to reduced gut microbial diversity, and proliferation or reduction in specific taxa. Therefore, future studies should include the whole community for a deeper understanding of this disease.

The usefulness of the gut microbiome as a tool towards targeted non-invasive biomarkers for IBD has been evaluated by compelling studies. An acceptable biomarker may help in early diagnosis and classification of IBD as well as in the prediction of disease outcome. Overall, IBD clinical management would benefit from the identification of microbiome-based biomarkers, which could provide less invasive assessment tools, enable personalized treatments, and reduce the health care economic burden associated with IBD. Collectively, these microbiome data represent a valuable data source that can be continually mined to identify associations between the microbiome and IBD for a deeper pathophysiological understanding which may promote the development of clinical strategies, including disease prevention, treatment, stratification and assessment of high-risk population.

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    Pérez-Brocal V., García-López R., Vázquez-Castellanos J.F., Nos P., Beltrán B., Latorre A., Moya A. Study of the viral and microbial communities associated with Crohn’s disease: A metagenomic approach. Clin. Transl. Gastroenterol. 2013;4:e36.

    Not in our library10.1038/ctg.2013.9

  30. 30.

    Kabeerdoss J., Jayakanthan P., Pugazhendhi S., Ramakrishna B.S. Alterations of mucosal microbiota in the colon of patients with inflammatory bowel disease revealed by real time polymerase chain reaction amplification of 16S ribosomal ribonucleic acid. Indian J. Med. Res. 2015;142:23-33.

    Not in our library10.4103/0971-5916.162091

  31. 31.

    Pérez-Brocal V., García-López R., Nos P., Beltrán B., Moret I., Moya A. Metagenomic analysis of Crohn’s disease patients identifies changes in the virome and microbiome related to disease status and therapy, and detects potential interactions and biomarkers. Inflamm. Bowel Dis. 2015;21:2515-2532.

    Not in our library10.1097/mib.0000000000000549

  32. 32.
    Intestinal Bacteria Composition and Translocation of Bacteria in Inflammatory Bowel Disease. · 2017
    Not checked
  33. 33.

    Rojas-feria M., Romero-garcía T., Caballero-rico J.Á.F., Ramírez H.P., Avilés-recio M., Castro-fernandez M., Porcuna N.C., Romero-gόmez M., García F., Grande L., et al. Modulation of faecal metagenome in Crohn’ s disease: Role of microRNAs as biomarkers. World J. Gastroenterol. 2018;24:5223-5233.

    Not in our library10.3748/wjg.v24.i46.5223

  34. 34.

    Vatn S., Carstens A., Kristoffersen A.B., Bergemalm D., Casén C., Moen A.E.F., Tannaes T.M., Lindstrøm J., Detlie T.E., Olbjørn C., et al. Faecal microbiota signatures of IBD and their relation to diagnosis, disease phenotype, inflammation, treatment escalation and anti-TNF response in a European Multicentre Study (IBD-Character). Scand. J. Gastroenterol. 2020;55:1146-1156.

    Not in our library10.1080/00365521.2020.1803396

  35. 35.

    Bibiloni R., Mangold M., Madsen K.L., Fedorak R.N., Tannock G.W. The bacteriology of biopsies differs between newly diagnosed, untreated, Crohn’s disease and ulcerative colitis patients. J. Med. Microbiol. 2006;55:1141-1149.

    Not in our library10.1099/jmm.0.46498-0

  36. 36.

    Moen A.E.F., Lindstrøm J.C., Tannæs T.M., Vatn S., Ricanek P., Vatn M.H., Jahnsen J., Frengen A.B., Dahl F.A., You P., et al. The prevalence and transcriptional activity of the mucosal microbiota of ulcerative colitis patients. Sci. Rep. 2018;8:17278.

    Not in our library10.1038/s41598-018-35243-4

  37. 37.

    Rubbens P., Props R., Kerckhof F.M., Boon N., Waegeman W. Cytometric fingerprints of gut microbiota predict Crohn’s disease state. ISME J. 2021;15:354-358.

    Not in our library10.1038/s41396-020-00762-4

  38. 38.

    Donaldson G.P., Lee S.M., Mazmanian S.K. Gut biogeography of the bacterial microbiota. Nat. Rev. Microbiol. 2015;14:20-32.

    Not in our library10.1038/nrmicro3552

  39. 39.

    Willing B.P., Dicksved J., Halfvarson J., Andersson A.F., Lucio M., Zheng Z., Järnerot G., Tysk C., Jansson J.K., Engstrand L. A pyrosequencing study in twins shows that gastrointestinal microbial profiles vary with inflammatory bowel disease phenotypes. Gastroenterology. 2010;139:1844-1854.

    Not in our library10.1053/j.gastro.2010.08.049

  40. 40.
    Characteristics of Fecal and Mucosa-Associated Microbiota in Chinese Patients With Inflammatory Bowel Disease · 2014
    No notice
  41. 41.

    Lepage P., Seksik P., Sutren M., de la Cochetière M.F., Jian R., Marteau P., Doré J. Biodiversity of the mucosa-associated microbiota is stable along the distal digestive tract in healthy individuals and patients with IBD. Inflamm. Bowel Dis. 2005;11:473-480.

    Not in our library10.1097/01.mib.0000159662.62651.06

  42. 42.

    Gillevet P., Sikaroodi M., Keshavarzian A., Mutlu E.A. Quantitative assessment of the human gut microbiome using multitag pyrosequencing. Chem. Biodivers. 2010;7:1065-1075.

    Not in our library10.1002/cbdv.200900322

  43. 43.

    Eun C.S., Kwak M.J., Han D.S., Lee A.R., Park D.I., Yang S.K., Kim Y.S., Kim J.F. Does the intestinal microbial community of Korean Crohn’s disease patients differ from that of western patients? BMC Gastroenterol. 2016;16:28.

    Not in our library10.1186/s12876-016-0437-0

  44. 44.

    Altomare A., Putignani L., Del Chierico F., Cocca S., Angeletti S., Ciccozzi M., Tripiciano C., Dalla Piccola B., Cicala M., Guarino M.P.L. Gut mucosal-associated microbiota better discloses inflammatory bowel disease differential patterns than faecal microbiota. Dig. Liver Dis. 2019;51:648-656.

    Not in our library10.1016/j.dld.2018.11.021

  45. 45.

    De Souza H.L., De Carvalho V.R., Romeiro F.G., Sassaki L.Y., Keller R., Rodrigues J. Mucosa-associated but not luminal Escherichia coli is augmented in Crohn’s disease and ulcerative colitis. Gut Pathog. 2012;4:21.

    Not in our library10.1186/1757-4749-4-21

  46. 46.

    Midtvedt T., Zabarovsky E., Norin E., Bark J., Gizatullin R., Kashuba V., Ljungqvist O., Zabarovska V., Möllby R., Ernberg I. Increase of faecal tryptic activity relates to changes in the intestinal microbiome: Analysis of Crohn’s disease with a multidisciplinary platform. PLoS ONE. 2013;8:e66074.

    Not in our library10.1371/journal.pone.0066074

  47. 47.

    Forbes J.D., Van Domselaar G., Bernstein C.N. Microbiome survey of the inflamed and noninflamed gut at different compartments within the gastrointestinal tract of inflammatory bowel disease patients. Inflamm. Bowel Dis. 2016;22:817-825.

    Not in our library10.1097/mib.0000000000000684

  48. 48.

    O’Brien C.L., Kiely C.J., Pavli P. The microbiome of Crohn’s disease aphthous ulcers. Gut Pathog. 2018;10:44.

    Not in our library10.1186/s13099-018-0265-6

  49. 49.

    Olaisen M., Flatberg A., Granlund A. van B.; Røyset, E.S.; Martinsen, T.C.; Sandvik, A.K.; Fossmark, R. Bacterial mucosa-associated microbiome in inflamed and proximal noninflamed ileum of patients with Crohn’s disease. Inflamm. Bowel Dis. 2020;27:12-24.

    Not in our library10.1093/ibd/izaa107

  50. 50.

    Zakrzewski M., Simms L.A., Brown A., Appleyard M., Irwin J., Waddell N., Radford-Smith G.L. IL23R-protective coding variant promotes beneficial bacteria and diversity in the ileal microbiome in healthy individuals without inflammatory bowel disease. J. Crohn’s Colitis. 2019;13:451-461.

    Not in our library10.1093/ecco-jcc/jjy188

  51. 51.

    Hirano A., Umeno J., Okamoto Y., Shibata H., Ogura Y., Moriyama T., Torisu T., Fujioka S., Fuyuno Y., Kawarabayasi Y., et al. Comparison of the microbial community structure between inflamed and non-inflamed sites in patients with ulcerative colitis. J. Gastroenterol. Hepatol. 2018;33:1590-1597.

    Not in our library10.1111/jgh.14129

  52. 52.
    High-throughput clone library analysis of the mucosa-associated microbiota reveals dysbiosis and differences between inflamed and non-inflamed regions of the intestine in inflammatory bowel disease · 2011
    No notice
  53. 53.

    Li Q., Wang C., Tang C., Li N., Li J. Molecular-phylogenetic characterization of the microbiota in ulcerated and non-ulcerated regions in the patients with crohn’s disease. PLoS ONE. 2012;7:e34939.

    Not in our library10.1371/journal.pone.0034939

  54. 54.

    Zhang M., Liu B., Zhang Y., Wei H., Lei Y., Zhao L. Structural shifts of mucosa-associated lactobacilli and Clostridium leptum subgroup in patients with ulcerative colitis. J. Clin. Microbiol. 2007;45:496-500.

    Not in our library10.1128/jcm.01720-06

  55. 55.

    Li E., Zhang Y., Tian X., Wang X., Gathungu G., Wolber A., Shiekh S.S., Sartor R.B., Davidson N.O., Ciorba M.A., et al. Influence of Crohn’s disease related polymorphisms in innate immune function on ileal microbiome. PLoS ONE. 2019;14:e0213108.

    Not in our library10.1371/journal.pone.0213108

  56. 56.
    Prevalence of Yersinia Species in the Ileum of Crohn's Disease Patients and Controls · 2018
    Not checked
  57. 57.
    Colonic microbiota is associated with inflammation and host epigenomic alterations in inflammatory bowel disease · 2020
    No notice
  58. 58.

    Libertucci J., Dutta U., Kaur S., Jury J., Rossi L., Fontes M.E., Shajib M.S., Khan W.I., Surette M.G., Verdu E.F., et al. Inflammation-related differences in mucosa-associated microbiota and intestinal barrier function in colonic Crohn’s disease. Am. J. Physiol. Gastrointest. Liver Physiol. 2018;315:G420-G431.

    Not in our library10.1152/ajpgi.00411.2017

  59. 59.

    Li Q., Wang C., Tang C., He Q., Li N., Li J. Dysbiosis of gut fungal microbiota is associated with mucosal inflammation in crohn’s disease. J. Clin. Gastroenterol. 2014;48:513-523.

    Not in our library10.1097/mcg.0000000000000035

  60. 60.

    Doolittle W.F., Booth A. It’s the song, not the singer: An exploration of holobiosis and evolutionary theory. Biol. Philos. 2017;32:5-24.

    Not in our library10.1007/s10539-016-9542-2

  61. 61.
    A Modular Organization of the Human Intestinal Mucosal Microbiota and Its Association with Inflammatory Bowel Disease · 2013
    No notice
  62. 62.

    Davenport M., Poles J., Leung J.M., Wolff M.J., Abidi W.M., Ullman T., Mayer L., Cho I., Loke P. Metabolic alterations to the mucosal microbiota in inflammatory bowel disease. Inflamm. Bowel Dis. 2014;20:723-731.

    Not in our library10.1097/mib.0000000000000011

  63. 63.

    Mobeen F., Sharma V., Prakash T. Enterotype variations of the healthy human gut microbiome in different geographical regions. Bioinformation. 2018;14:560-573.

    Not in our library10.6026/97320630014560

  64. 64.

    Bäckhed F., Fraser C.M., Ringel Y., Sanders M.E., Sartor R.B., Sherman P.M., Versalovic J., Young V., Finlay B.B. Defining a healthy human gut microbiome: Current concepts, future directions, and clinical applications. Cell Host Microbe. 2012;12:611-622.

    Not in our library10.1016/j.chom.2012.10.012

  65. 65.

    Frank D.N., Amand A.L.S., Feldman R.A., Boedeker E.C., Harpaz N., Pace N.R. Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc. Natl. Acad. Sci. USA. 2007;104:13780-13785.

    Not in our library10.1073/pnas.0706625104

  66. 66.
    Cross sectional evaluation of the gut-microbiome metabolome axis in an Italian cohort of IBD patients · 2017
    Corrected
  67. 67.

    Lo Sasso G., Khachatryan L., Kondylis A., Battey J.N.D., Solovyeva V.V., Garanina E.E., Kitaeva K.V., Ivanov K.Y. Inflammatory bowel disease—Associated changes in the gut: Focus on Kazan patients. Inflamm. Bowel Dis. 2020;27:418-433.

    Not in our library10.1093/ibd/izaa188

  68. 68.
    Microbial imbalance in inflammatory bowel disease patients at different taxonomic levels · 2020
    No notice
  69. 69.

    Manichanh C., Bonnaud E., Gloux K., Pelletier E., Frangeul L., Nalin R., Jarrin C., Chardon P., Marteau P., Roca J., et al. Reduced diversity of faecal microbiota in Crohn’s disease revealed by a metagenomic approach. Gut. 2006;55:205-211.

    Not in our library10.1136/gut.2005.073817

  70. 70.

    Mondot S., Kang S., Furet J.P., Aguirre De Carcer D., McSweeney C., Morrison M., Marteau P., Doré J., Leclerc M. Highlighting new phylogenetic specificities of Crohn’s disease microbiota. Inflamm. Bowel Dis. 2011;17:185-192.

    Not in our library10.1002/ibd.21436

  71. 71.
    Metagenomic Characterization of Microbial Communities In Situ Within the Deeper Layers of the Ileum in Crohnâs DiseaseSummary · 2016
    Not checked
  72. 72.

    Moustafa A., Li W., Anderson E.L., Wong E.H.M., Dulai P.S., Sandborn W.J., Biggs W., Yooseph S., Jones M.B., Venter J.C., et al. Genetic risk, dysbiosis, and treatment stratification using host genome and gut microbiome in inflammatory bowel disease. Clin. Transl. Gastroenterol. 2018;9:e132.

    Not in our library10.1038/ctg.2017.58

  73. 73.

    Duboc H., Rajca S., Rainteau D., Benarous D., Maubert M.A., Quervain E., Thomas G., Barbu V., Humbert L., Despras G., et al. Connecting dysbiosis, bile-acid dysmetabolism and Gut inflammation in inflammatory bowel diseases. Gut. 2012;62:531-539.

    Not in our library10.1136/gutjnl-2012-302578

  74. 74.

    Vidal R., Ginard D., Khorrami S., Mora-Ruiz M., Munoz R., Hermoso M., Díaz S., Cifuentes A., Orfila A., Rosselló-Móra R. Crohn associated microbial communities associated to colonic mucosal biopsies in patients of the western Mediterranean. Syst. Appl. Microbiol. 2015;38:442-452.

    Not in our library10.1016/j.syapm.2015.06.008

  75. 75.

    Borren N.Z., Plichta D., Joshi A.D., Bonilla G., Sadreyev R., Vlamakis H., Xavier R.J., Ananthakrishnan A.N. Multi-“-omics” profiling in patients with quiescent inflammatory bowel disease identifies biomarkers predicting relapse. Inflamm. Bowel Dis. 2020;26:1524-1532.

    Not in our library10.1093/ibd/izaa183

  76. 76.

    Clooney A.G., Eckenberger J., Laserna-Mendieta E., Sexton K.A., Bernstein M.T., Vagianos K., Sargent M., Ryan F.J., Moran C., Sheehan D., et al. Ranking microbiome variance in inflammatory bowel disease: A large longitudinal intercontinental study. Gut. 2020;70:499-510.

    Not in our library10.1136/gutjnl-2020-321106

  77. 77.

    Kennedy N.A., Lamb C.A., Berry S.H., Walker A.W., Mansfield J., Parkes M., Simpkins R., Tremelling M., Nutland S., Parkhill J., et al. The impact of NOD2 variants on fecal microbiota in Crohn’s disease and controls without gastrointestinal disease. Inflamm. Bowel Dis. 2018;24:583-592.

    Not in our library10.1093/ibd/izx061

  78. 78.

    Kleessen B., Kroesen A.J., Buhr H.J., Blaut M. Mucosal and invading bacteria in patients with inflammatory bowel disease compared with controls. Scand. J. Gastroenterol. 2002;37:1034-1041.

    Not in our library10.1080/003655202320378220

  79. 79.

    Gophna U., Sommerfeld K., Gophna S., Doolittle W.F., Van Zanten S.J.O.V. Differences between Tissue-Associated Intestinal Microfloras of Patients with Crohn’ s Disease and Ulcerative Colitis. J. Clin. Microbiol. 2006;44:4136-4141.

    Not in our library10.1128/jcm.01004-06

  80. 80.

    Kang S., Denman S.E., Morrison M., Yu Z., Dore J., Leclerc M., McSweeney C.S. Dysbiosis of fecal microbiota in Crohn’s disease patients as revealed by a custom phylogenetic microarray. Inflamm. Bowel Dis. 2010;16:2034-2042.

    Not in our library10.1002/ibd.21319

  81. 81.

    Nishino K., Nishida A., Inoue R., Kawada Y., Ohno M., Sakai S., Inatomi O., Bamba S., Sugimoto M., Kawahara M., et al. Analysis of endoscopic brush samples identified mucosa-associated dysbiosis in inflammatory bowel disease. J. Gastroenterol. 2018;53:95-106.

    Not in our library10.1007/s00535-017-1384-4

  82. 82.
    Increased abundance of proteobacteria in aggressive Crohn’s disease seven years after diagnosis · 2019
    No notice
  83. 83.

    Rowan F., Docherty N.G., Murphy M., Murphy B., Coffey J.C., O’Connell P.R. Desulfovibrio bacterial species are increased in ulcerative colitis. Dis. Colon Rectum. 2010;53:1530-1536.

    Not in our library10.1007/dcr.0b013e3181f1e620

  84. 84.

    Lennon G., Balfe Á., Bambury N., Lavelle A., Maguire A., Docherty N.G., Coffey J.C., Winter D.C., Sheahan K., O’Connell P.R. Correlations between colonic crypt mucin chemotype, inflammatory grade and Desulfovibrio species in ulcerative colitis. Color. Dis. 2014;16:161-169.

    Not in our library10.1111/codi.12503

  85. 85.

    Al-Bayati L., Fasaei B.N., Merat S., Bahonar A. Longitudinal analyses of Gut-associated bacterial microbiota in ulcerative colitis patients. Arch. Iran. Med. 2018;21:578-584.

    Not in our library

  86. 86.

    Machiels K., Joossens M., Sabino J., De Preter V., Arijs I., Eeckhaut V., Ballet V., Claes K., Van Immerseel F., Verbeke K., et al. A decrease of the butyrate-producing species Roseburia hominis and Faecalibacterium prausnitzii defines dysbiosis in patients with ulcerative colitis. Gut. 2014;63:1275-1283.

    Not in our library10.1136/gutjnl-2013-304833

  87. 87.

    Varela E., Manichanh C., Gallart M., Torrejon A., Borruel N., Casellas F., Guarner F., Antolin M. Colonisation by Faecalibacterium prausnitzii and maintenance of clinical remission in patients with ulcerative colitis. Aliment. Pharmacol. Ther. 2013;38:151-161.

    Not in our library10.1111/apt.12365

  88. 88.

    Pascal V., Pozuelo M., Borruel N., Casellas F., Campos D., Santiago A., Martinez X., Varela E., Sarrabayrouse G., Machiels K., et al. A microbial signature for Crohn’s disease. Gut. 2017;66:813-822.

    Not in our library10.1136/gutjnl-2016-313235

  89. 89.

    Yilmaz B., Juillerat P., Øyås O., Ramon C., Bravo F.D., Franc Y., Fournier N., Michetti P., Mueller C., Geuking M., et al. Microbial network disturbances in relapsing refractory Crohn’s disease. Nat. Med. 2019;25:323-336.

    Not in our library10.1038/s41591-018-0308-z

  90. 90.

    Sokol H., Seksik P., Rigottier-gois L., Lay C., Lepage P., Podglajen I., Marteau P. Specificities of the fecal microbiota in inflammatory bowel disease. Inflamm. Bowel Dis. 2006;12:106-111.

    Not in our library10.1097/01.mib.0000200323.38139.c6

  91. 91.

    Sokol H., Pigneur B., Watterlot L., Lakhdari O., Bermúdez-Humarán L.G., Gratadoux J.J., Blugeon S., Bridonneau C., Furet J.P., Corthier G., et al. Faecalibacterium prausnitzii is an anti-inflammatory commensal bacterium identified by gut microbiota analysis of Crohn disease patients. Proc. Natl. Acad. Sci. USA. 2008;105:16731-16736.

    Not in our library10.1073/pnas.0804812105

  92. 92.

    Zhang Y.-L., Cai L.-T., Qi J.-Y., Lin Y.-Z., Dai Y.-C., Jiao N., Chen Y.-L., Zheng L., Wang B.-B., Zhu L.-X., et al. Gut microbiota contributes to the distinction between two traditional Chinese medicine syndromes of ulcerative colitis. World J. Gastroenterol. 2019;25:3108-3282.

    Not in our library10.3748/wjg.v25.i25.3242

  93. 93.

    Takahashi K., Nishida A., Fujimoto T., Fujii M., Shioya M., Imaeda H., Inatomi O., Bamba S., Andoh A., Sugimoto M. Reduced abundance of butyrate-producing bacteria species in the fecal microbial community in Crohn’s disease. Digestion. 2016;93:59-65.

    Not in our library10.1159/000441768

  94. 94.

    Imhann F., Vila A.V., Bonder M.J., Fu J., Gevers D., Visschedijk M.C., Spekhorst L.M., Alberts R., Franke L., van Dullemen H.M., et al. Interplay of host genetics and gut microbiota underlying the onset and clinical presentation of inflammatory bowel disease. Gut. 2018;67:108-119.

    Not in our library10.1136/gutjnl-2016-312135

  95. 95.

    Kumari R., Ahuja V., Paul J. Fluctuations in butyrate-producing bacteria in ulcerative colitis patients of North India. World J. Gastroenterol. 2013;19:3404-3414.

    Not in our library10.3748/wjg.v19.i22.3404

  96. 96.
    Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases · 2019
    Corrected
  97. 97.

    Joossens M., Huys G., Cnockaert M., De Preter V., Verbeke K., Rutgeerts P., Vandamme P., Vermeire S. Dysbiosis of the faecal microbiota in patients with Crohn’s disease and their unaffected relatives. Gut. 2011;60:631-637.

    Not in our library10.1136/gut.2010.223263

  98. 98.
    A novel Ruminococcus gnavus clade enriched in inflammatory bowel disease patients · 2017
    No notice
  99. 99.
    Bacteriome and Mycobiome Interactions Underscore Microbial Dysbiosis in Familial Crohn’s Disease · 2016
    No notice
  100. 100.

    Underhill D.M., Iliev I.D. The mycobiota: Interactions between commensal fungi and the host immune system. Nat. Rev. Immunol. 2014;14:405-416.

    Not in our library10.1038/nri3684

  101. 101.

    McKenzie H., Main J., Pennington C.R., Parratt D. Antibody to selected strains of Sacharomyces cerevisiae (baker’s and brewer’s yeast) and Candida albicans in Crohn’s disease. Gut. 1990;31:536-538.

    Not in our library10.1136/gut.31.5.536

  102. 102.

    Qin J., Li R., Raes J., Arumugam M., Burgdorf S., Manichanh C., Nielsen T., Pons N., Yamada T., Mende D.R., et al. A human gut microbial gene catalog established by metagenomic sequencing. Nature. 2010;464:59-65.

    Not in our library10.1038/nature08821

  103. 103.

    Qiu X., Ma J., Jiao C., Mao X., Zhao X., Lu M., Wang K., Zhang H. Alterations in the mucosa-associated fungal microbiota in patients with ulcerative colitis. Oncotarget. 2017;8:107577-107588.

    Not in our library10.18632/oncotarget.22534

  104. 104.

    Sokol H., Leducq V., Aschard H., Pham H.P., Jegou S., Landman C., Cohen D., Liguori G., Bourrier A., Nion-Larmurier I., et al. Fungal microbiota dysbiosis in IBD. Gut. 2016;66:1039-1048.

    Not in our library10.1136/gutjnl-2015-310746

  105. 105.

    Ott S.J., Kühbacher T., Musfeldt M., Rosenstiel P., Hellmig S., Rehman A., Drews O., Weichert W., Timmis K.N., Schreiber S. Fungi and inflammatory bowel diseases: Alterations of composition and diversity. Scand. J. Gastroenterol. 2008;43:831-841.

    Not in our library10.1080/00365520801935434

  106. 106.

    Imai T., Inoue R., Kawada Y., Morita Y., Inatomi O., Nishida A., Bamba S., Kawahara M., Andoh A. Characterization of fungal dysbiosis in Japanese patients with inflammatory bowel disease. J. Gastroenterol. 2019;54:149-159.

    Not in our library10.1007/s00535-018-1530-7

  107. 107.

    Liguori G., Lamas B., Richard M.L., Brandi G., da Costa G., Hoffmann T.W., Di Simone M.P., Calabrese C., Poggioli G., Langella P., et al. Fungal dysbiosis in mucosa-associated microbiota of Crohn’s disease patients. J. Crohn’s Colitis. 2016;10:296-305.

    Not in our library10.1093/ecco-jcc/jjv209

  108. 108.

    Mar J.S., Lamere B.J., Lin D.L., Levan S., Nazareth M., Mahadevan U., Lynch S.V. Disease severity and immune activity relate to distinct interkingdom gut microbiome states in ethnically distinct ulcerative colitis patients. MBio. 2016;7:e01072-16.

    Not in our library10.1128/mbio.01072-16

  109. 109.

    Shkoporov A.N., Clooney A.G., Sutton T.D.S., Ryan F.J., Daly K.M., Nolan J.A., McDonnell S.A., Khokhlova E.V., Draper L.A., Forde A., et al. The human gut virome is highly diverse, stable, and individual specific. Cell Host Microbe. 2019;26:527-541.e5.

    Not in our library10.1016/j.chom.2019.09.009

  110. 110.

    Clooney A.G., Sutton T.D.S., Shkoporov A.N., Holohan R.K., Daly K.M., O’Regan O., Ryan F.J., Draper L.A., Plevy S.E., Ross R.P., et al. Whole-virome analysis sheds light on viral dark matter in inflammatory bowel disease. Cell Host Microbe. 2019;26:764-778.e5.

    Not in our library10.1016/j.chom.2019.10.009

  111. 111.

    Wang W., Jovel J., Halloran B., Wine E., Patterson J., Ford G., O’Keefe S., Meng B., Song D., Zhang Y., et al. Metagenomic analysis of microbiome in colon tissue from subjects with inflammatory bowel diseases reveals interplay of viruses and bacteria. Inflamm. Bowel Dis. 2015;21:1419-1427.

    Not in our library10.1097/mib.0000000000000344

  112. 112.

    Zuo T., Lu X.J., Zhang Y., Cheung C.P., Lam S., Zhang F., Tang W., Ching J.Y.L., Zhao R., Chan P.K.S., et al. Gut mucosal virome alterations in ulcerative colitis. Gut. 2019;68:1169-1179.

    Not in our library10.1136/gutjnl-2018-318131

  113. 113.

    Norman J.M., Handley S.A., Baldridge M.T., Droit L., Catherine Y., Keller B.C., Kambal A., Zhao G., Stappenbeck T.S., Mcgovern D.P.B., et al. Disease-specific alterations in the enteric virome in inflammatory bowel disease. Cell. 2015;160:447-460.

    Not in our library10.1016/j.cell.2015.01.002

  114. 114.

    Dridi B., Raoult D., Drancourt M. Archaea as emerging organisms in complex human microbiomes. Anaerobe. 2011;17:56-63.

    Not in our library10.1016/j.anaerobe.2011.03.001

  115. 115.

    Ghavami S.B., Rostami E., Sephay A.A., Shahrokh S., Balaii H., Aghdaei H.A., Zali M.R. Alterations of the human gut Methanobrevibacter smithii as a biomarker for inflammatory bowel diseases. Microb. Pathog. 2018;117:285-289.

    Not in our library10.1016/j.micpath.2018.01.029

  116. 116.
    Increased Prevalence of Methanosphaera stadtmanae in Inflammatory Bowel Diseases · 2014
    No notice
  117. 117.

    Sun M., Du B., Shi Y., Lu Y., Zhou Y., Liu B. Combined signature of the fecal microbiome and plasma metabolome in patients with ulcerative colitis. Med. Sci. Monit. 2019;25:3303-3315.

    Not in our library10.12659/msm.916009

  118. 118.

    Wang W., Chen L., Zhou R., Wang X., Song L., Huang S., Wang G., Xia B. Increased proportions of bifidobacterium and the lactobacillus group and loss of butyrate-producing bacteria in inflammatory bowel. J. Clin. Microbiol. 2014;52:398-406.

    Not in our library10.1128/jcm.01500-13

  119. 119.

    Braun T., Di Segni A., Benshoshan M., Neuman S., Levhar N., Bubis M., Picard O., Sosnovski K., Efroni G., Farage Barhom S., et al. Individualized dynamics in the gut microbiota precede Crohn’s disease flares. Am. J. Gastroenterol. 2019;114:1142-1151.

    Not in our library10.14309/ajg.0000000000000136

  120. 120.

    Fite A., Macfarlane S., Furrie E., Bahrami B., Cummings J.H., Steinke D.T., MacFarlane G.T. Longitudinal analyses of gut mucosal microbiotas in ulcerative colitis in relation to patient age and disease severity and duration. J. Clin. Microbiol. 2013;51:849-856.

    Not in our library10.1128/jcm.02574-12

  121. 121.

    Zhang J., Chen S.L., Li L.B. Correlation between intestinal flora and serum inflammatory factors in patients with Crohn’s disease. Eur. Rev. Med. Pharmacol. Sci. 2017;21:4913-4917.

    Not in our library

  122. 122.

    Ji Y., Li X., Zhu Y., Li N., Zhang N., Niu M. Faecal microRNA as a biomarker of the activity and prognosis of inflammatory bowel diseases. Biochem. Biophys. Res. Commun. 2018;503:2443-2450.

    Not in our library10.1016/j.bbrc.2018.06.174

  123. 123.

    Andoh A., Kuzuoka H., Tsujikawa T., Nakamura S. Multicenter analysis of fecal microbiota profiles in Japanese patients with Crohn’ s disease. J. Gastroenterol. 2012;47:1298-1307.

    Not in our library10.1007/s00535-012-0605-0

  124. 124.

    Sha S., Xu B., Wang X., Zhang Y., Wang H., Kong X., Zhu H., Wu K. The biodiversity and composition of the dominant fecal microbiota in patients with inflammatory bowel disease. Diagn. Microbiol. Infect. Dis. 2013;75:245-251.

    Not in our library10.1016/j.diagmicrobio.2012.11.022

  125. 125.

    Naftali T., Reshef L., Kovacs A., Porat R., Amir I., Konikoff F.M., Gophna U. Distinct microbiotas are associated with ileum-restricted and colon-involving Crohn’s disease. Inflamm. Bowel Dis. 2016;22:293-302.

    Not in our library10.1097/mib.0000000000000662

  126. 126.

    Nemoto H., Kataoka K., Ishikawa H., Ikata K., Arimochi H., Iwasaki T., Ohnishi Y., Kuwahara T., Yasutomo K. Reduced diversity and imbalance of fecal microbiota in patients with ulcerative colitis. Dig. Dis. Sci. 2012;57:2955-2964.

    Not in our library10.1007/s10620-012-2236-y

  127. 127.
    Clostridium leptum group bacteria abundance and diversity in the fecal microbiota of patients with inflammatory bowel disease: a case–control study in India · 2013
    No notice
  128. 128.

    Heidarian F., Alebouyeh M., Shahrokh S., Balaii H., Zali M.R. Altered fecal bacterial composition correlates with disease activity in inflammatory bowel disease and the extent of IL8 induction. Curr. Res. Transl. Med. 2019;67:41-50.

    Not in our library10.1016/j.retram.2019.01.002

  129. 129.

    Boland K., Bedrani L., Turpin W., Kabakchiev B., Stempak J., Borowski K., Nguyen G., Steinhart A.H., Smith M.I., Croitoru K., et al. Persistent diarrhea in patients with Crohn’s disease after mucosal healing is associated with lower diversity of the intestinal microbiome and increased dysbiosis. Clin. Gastroenterol. Hepatol. 2020;19:296-304.e3.

    Not in our library10.1016/j.cgh.2020.03.044

  130. 130.

    Walujkar S.A., Kumbhare S.V., Marathe N.P., Patangia D.V., Lawate P.S., Bharadwaj R.S., Shouche Y.S. Molecular profiling of mucosal tissue associated microbiota in patients manifesting acute exacerbations and remission stage of ulcerative colitis. World J. Microbiol. Biotechnol. 2018;34:76.

    Not in our library10.1007/s11274-018-2449-0

  131. 131.

    Mitsuyama K., Niwa M., Takedatsu H., Yamasaki H., Kuwaki K., Yoshioka S., Yamauchi R., Fukunaga S., Torimura T. Antibody markers in the diagnosis of inflammatory bowel disease. World J. Gastroenterol. 2016;22:1304-1310.

    Not in our library10.3748/wjg.v22.i3.1304

  132. 132.

    Gisbert J.P., Gomollón F., Maté J., Pajares J.M. Papel de los anticuerpos anticitoplasma de los neutrófilos (ANCA) y anti-Saccharomyces cerevisiae (ASCA) en la enfermedad inflamatoria intestinal. Gastroenterol. Hepatol. 2003;26:312-324.

    Not in our library10.1016/s0210-5705(03)70365-3

  133. 133.

    Li Y., Hauenstein K. New imaging techniques in the diagnosis of inflammatory bowel diseases. Visz. Gastrointest. Med. Surg. 2015;31:227-234.

    Not in our library10.1159/000435864

  134. 134.

    Lopez R.N., Leach S.T., Lemberg D.A., Duvoisin G., Gearry R.B., Day A.S. Fecal biomarkers in inflammatory bowel disease. J. Gastroenterol. Hepatol. 2017;32:577-582.

    Not in our library10.1111/jgh.13611

  135. 135.

    Tedjo D.I., Smolinska A., Savelkoul P.H., Masclee A.A., Van Schooten F.J., Pierik M.J., Penders J., Jonkers D.M.A.E. The fecal microbiota as a biomarker for disease activity in Crohn’s disease. Sci. Rep. 2016;6:35216.

    Not in our library10.1038/srep35216

  136. 136.

    Rehman A., Rausch P., Wang J., Skieceviciene J., Kiudelis G., Bhagalia K., Amarapurkar D., Kupcinskas L., Schreiber S., Rosenstiel P., et al. Geographical patterns of the standing and active human gut microbiome in health and IBD. Gut. 2016;65:238-248.

    Not in our library10.1136/gutjnl-2014-308341

  137. 137.

    Willing B., Halfvarson J., Dicksved J., Rosenquist M., Järnerot G., Engstrand L., Tysk C., Jansson J.K. Twin studies reveal specific imbalances in the mucosa-associated microbiota of patients with ileal Crohn’s disease. Inflamm. Bowel Dis. 2009;15:653-660.

    Not in our library10.1002/ibd.20783

  138. 138.

    Wisittipanit N., Rangwala H., Sikaroodi M., Keshavarzian A., Mutlu E.A., Gillevet P. Classification methods for the analysis of LH-PCR data associated with inflammatory bowel disease patients. Int. J. Bioinform. Res. Appl. 2015;11:111-129.

    Not in our library10.1504/ijbra.2015.068087

  139. 139.

    Fukuda K., Fujita Y. Determination of the discriminant score of intestinal microbiota as a biomarker of disease activity in patients with ulcerative colitis. BMC Gastroenterol. 2014;14:49.

    Not in our library10.1186/1471-230x-14-49

  140. 140.

    Andoh A., Kobayashi T., Kuzuoka H., Tsujikawa T., Suzuki Y., Hirai F., Matsui T., Nakamura S., Matsumoto T., Fujiyama Y. Characterization of gut microbiota profiles by disease activity in patients with Crohn’s disease using data mining analysis of terminal restriction fragment length polymorphisms. Biomed. Rep. 2014;2:370-373.

    Not in our library10.3892/br.2014.252

  141. 141.

    Butera A., Di Paola M., Vitali F., De Nitto D., Covotta F., Borrini F., Pica R., De Filippo C., Cavalieri D., Giuliani A., et al. IL-13 mRNA tissue content identifies two subsets of adult ulcerative colitis patients with different clinical and mucosa-associated microbiota profiles. J. Crohn’s Colitis. 2020;14:369-380.

    Not in our library10.1093/ecco-jcc/jjz154

  142. 142.

    Macfarlane S., Furrie E., Cummings J.H., Macfarlane G.T. Chemotaxonomic analysis of bacterial populations colonizing the rectal mucosa in patients with ulcerative colitis. Clin. Infect. Dis. 2004;38:1690-1699.

    Not in our library10.1086/420823

  143. 143.

    Sokol H., Lepage P., Seksik P., Dore J., Marteau P. Temperature gradient gel electrophoresis of fecal 16S rRNA reveals active escherichia coli in the microbiota of patients with ulcerative colitis. J. Clin. Microbiol. 2006;44:3172-3177.

    Not in our library10.1128/jcm.02600-05

  144. 144.

    Sepehri S., Kotlowski R., Bernstein C.N., Krause D.O. Microbial diversity of inflamed and noninflamed gut biopsy tissues in inflammatory bowel disease. Inflamm. Bowel Dis. 2007;13:675-683.

    Not in our library10.1002/ibd.20101

  145. 145.

    Andoh A., Sakata S., Koizumi Y., Mitsuyama K., Fujiyama Y., Benno Y. Terminal restriction fragment length polymorphism analysis of the diversity of fecal microbiota in patients with ulcerative colitis. Inflamm. Bowel Dis. 2007;13:955-962.

    Not in our library10.1002/ibd.20151

  146. 146.

    Dicksved J., Halfvarson J., Rosenquist M., Järnerot G., Tysk C., Apajalahti J., Engstrand L., Jansson J.K. Molecular analysis of the gut microbiota of identical twins with Crohn’s disease. ISME J. 2008;2:716-727.

    Not in our library10.1038/ismej.2008.37

  147. 147.

    Kuehbacher T., Rehman A., Lepage P., Hellmig S., Fölsch U.R., Schreiber S., Ott S.J. Intestinal TM7 bacterial phylogenies in active inflammatory bowel disease. J. Med. Microbiol. 2008;57:1569-1576.

    Not in our library10.1099/jmm.0.47719-0

  148. 148.

    Andoh A., Tsujikawa T., Sasaki M., Mitsuyama K., Suzuki Y., Matsui T., Matsumoto T., Benno Y., Fujiyama Y. Faecal microbiota profile of Crohn’s disease determined by terminal restriction fragment length polymorphism analysis. Aliment. Pharmacol. Ther. 2008;29:75-82.

    Not in our library10.1111/j.1365-2036.2008.03860.x

  149. 149.

    Nishikawa J., Kudo T., Sakata S., Benno Y., Sugiyama T. Diversity of mucosa-associated microbiota in active and inactive ulcerative colitis. Scand. J. Gastroenterol. 2009;44:180-186.

    Not in our library10.1080/00365520802433231

  150. 150.

    Andoh A., Ida S., Tsujikawa T., Benno Y., Fujiyama Y. Terminal restriction fragment polymorphism analyses of fecal microbiota in five siblings including two with ulcerative colitis. Clin. J. Gastroenterol. 2009;2:343-345.

    Not in our library10.1007/s12328-009-0106-8

  151. 151.

    Rehman A., Lepage P., Nolte A., Hellmig S., Schreiber S., Ott S.J. Transcriptional activity of the dominant gut mucosal microbiota in chronic inflammatory bowel disease patients. J. Med. Microbiol. 2010;59:1114-1122.

    Not in our library10.1099/jmm.0.021170-0

  152. 152.

    Andoh A., Imaeda H., Aomatsu T., Inatomi O., Bamba S., Sasaki M., Saito Y., Tsujikawa T., Fujiyama Y. Comparison of the fecal microbiota profiles between ulcerative colitis and Crohn’s disease using terminal restriction fragment length polymorphism analysis. J. Gastroenterol. 2011;46:479-486.

    Not in our library10.1007/s00535-010-0368-4

  153. 153.

    Lepage P., Hösler R., Spehlmann M.E., Rehman A., Zvirbliene A., Begun A., Ott S., Kupcinskas L., Doré J., Raedler A., et al. Twin study indicates loss of interaction between microbiota and mucosa of patients with ulcerative colitis. Gastroenterology. 2011;141:227-236.

    Not in our library10.1053/j.gastro.2011.04.011

  154. 154.

    Benjamin J.L., Hedin C.R.H., Koutsoumpas A., Ng S.C., McCarthy N.E., Prescott N.J., Pessoa-Lopes P., Mathew C.G., Sanderson J., Hart A.L., et al. Smokers with active Crohn’s disease have a clinically relevant dysbiosis of the gastrointestinal microbiota. Inflamm. Bowel Dis. 2012;18:1092-1100.

    Not in our library10.1002/ibd.21864

  155. 155.

    Hotte N.S.C., Salim S.Y., Tso R.H., Albert E.J., Bach P., Walker J., Dieleman L.A., Fedorak R.N., Madsen K.L. Patients with inflammatory bowel disease exhibit dysregulated responses to microbial DNA. PLoS ONE. 2012;7:e37932.

    Not in our library10.1371/journal.pone.0037932

  156. 156.

    Pistone D., Marone P., Pajoro M., Fabbi M., Vicari N., Daffara S., Dalla Valle C., Gabba S., Sassera D., Verri A., et al. Mycobacterium avium paratuberculosis in Italy: Commensal or emerging human pathogen? Dig. Liver Dis. 2012;44:461-465.

    Not in our library10.1016/j.dld.2011.12.022

  157. 157.

    Vigsnæs L.K., Brynskov J., Steenholdt C., Wilcks A., Licht T.R. Gram-negative bacteria account for main differences between faecal microbiota from patients with ulcerative colitis and healthy controls. Benef. Microbes. 2012;3:287-297.

    Not in our library10.3920/bm2012.0018

  158. 158.

    Fujimoto T., Imaeda H., Takahashi K., Kasumi E., Bamba S., Fujiyama Y., Andoh A. Decreased abundance of Faecalibacterium prausnitzii in the gut microbiota of Crohn’s disease. J. Gastroenterol. Hepatol. 2013;28:613-619.

    Not in our library10.1111/jgh.12073

  159. 159.

    Rajilić-Stojanović M., Shanahan F., Guarner F., De Vos W.M. Phylogenetic analysis of dysbiosis in ulcerative colitis during remission. Inflamm. Bowel Dis. 2013;19:481-488.

    Not in our library10.1097/mib.0b013e31827fec6d

  160. 160.

    Hedin C.R., McCarthy N.E., Louis P., Farquharson F.M., McCartney S., Taylor K., Prescott N.J., Murrells T., Stagg A.J., Whelan K., et al. Altered intestinal microbiota and blood T cell phenotype are shared by patients with Crohn’s disease and their unaffected siblings. Gut. 2014;63:1578-1586.

    Not in our library10.1136/gutjnl-2013-306226

  161. 161.

    Takeshita K., Mizuno S., Mikami Y., Sujino T., Saigusa K., Matsuoka K., Naganuma M., Sato T., Takada T., Tsuji H., et al. A single species of clostridium Subcluster XIVa decreased in ulcerative colitis patients. Inflamm. Bowel Dis. 2016;22:2802-2810.

    Not in our library10.1097/mib.0000000000000972

  162. 162.

    Zamani S., Hesam Shariati S., Zali M.R., Asadzadeh Aghdaei H., Sarabi Asiabar A., Bokaie S., Nomanpour B., Sechi L.A., Feizabadi M.M. Detection of enterotoxigenic Bacteroides fragilis in patients with ulcerative colitis. Gut Pathog. 2017;9:53.

    Not in our library10.1186/s13099-017-0202-0

  163. 163.

    Rausch P., Rehman A., Künzel S., Häsler R., Ott S.J., Schreiber S., Rosenstiel P., Franke A., Baines J.F. Colonic mucosa-associated microbiota is influenced by an interaction of crohn disease and FUT2 (Secretor) genotype. Proc. Natl. Acad. Sci. USA. 2011;108:19030-19035.

    Not in our library10.1073/pnas.1106408108

  164. 164.
    Integrated Metagenomics/Metaproteomics Reveals Human Host-Microbiota Signatures of Crohn's Disease · 2012
    No notice
  165. 165.
    Inflammatory Bowel Diseases Phenotype, C. difficile and NOD2 Genotype Are Associated with Shifts in Human Ileum Associated Microbial Composition · 2012
    No notice
  166. 166.

    Prideaux L., Kang S., Wagner J., Buckley M., Mahar J.E., De Cruz P., Wen Z., Chen L., Xia B., Van Langenberg D.R., et al. Impact of ethnicity, geography, and disease on the microbiota in health and inflammatory bowel disease. Inflamm. Bowel Dis. 2013;19:2906-2918.

    Not in our library10.1097/01.mib.0000435759.05577.12

  167. 167.

    Chiodini R.J., Dowd S.E., Davis B., Galandiuk S., Chamberlin W.M., Kuenstner J.T., McCallum R.W., Zhang J. Crohn’s disease may be differentiated into 2 distinct biotypes based on the detection of bacterial genomic sequences and virulence genes within submucosal tissues. J. Clin. Gastroenterol. 2013;47:612-620.

    Not in our library10.1097/mcg.0b013e31827b4f94

  168. 168.

    Lavelle A., Lennon G., O’Sullivan O., Docherty N., Balfe A., Maguire A., Mulcahy H.E., Doherty G., O’Donoghue D., Hyland J., et al. Spatial variation of the colonic microbiota in patients with ulcerative colitis and control volunteers. Gut. 2015;64:1553-1561.

    Not in our library10.1136/gutjnl-2014-307873

  169. 169.
    Microbial Population Differentials between Mucosal and Submucosal Intestinal Tissues in Advanced Crohn's Disease of the Ileum · 2015
    No notice
  170. 170.

    Chiodini R.J., Dowd S.E., Galandiuk S., Davis B., Glassing A. The predominant site of bacterial translocation across the intestinal mucosal barrier occurs at the advancing disease margin in Crohn’s disease. Microbiology. 2016;162:1608-1619.

    Not in our library10.1099/mic.0.000336

  171. 171.

    Hedin C., Van Der Gast C.J., Rogers G.B., Cuthbertson L., McCartney S., Stagg A.J., Lindsay J.O., Whelan K. Siblings of patients with Crohn’s disease exhibit a biologically relevant dysbiosis in mucosal microbial metacommunities. Gut. 2016;65:944-953.

    Not in our library10.1136/gutjnl-2014-308896

  172. 172.

    Chen G., Zhang Y., Wang W., Ji X., Meng F., Xu P., Yang N., Ye F., Bo X. Partners of patients with ulcerative colitis exhibit a biologically relevant dysbiosis in fecal microbial metacommunities. World J. Gastroenterol. 2017;23:4624-4631.

    Not in our library10.3748/wjg.v23.i25.4624

  173. 173.

    Chiodini R.J., Dowd S.E., Barron J.N., Galandiuk S., Davis B., Glassing A. Transitional and temporal changes in the mucosal and submucosal intestinal microbiota in advanced crohn’s disease of the terminal ileum. J. Med. Microbiol. 2018;67:549-559.

    Not in our library10.1099/jmm.0.000690

  174. 174.

    Ma H.Q., Yu T.T., Zhao X.J., Zhang Y., Zhang H.J. Fecal microbial dysbiosis in Chinese patients with inflammatory bowel disease. World J. Gastroenterol. 2018;24:1464-1477.

    Not in our library10.3748/wjg.v24.i13.1464

  175. 175.

    Laserna-Mendieta E.J., Clooney A.G., Carretero-Gomez J.F., Moran C., Sheehan D., Nolan J.A., Hill C., Gahan C.G.M., Joyce S.A., Shanahan F., et al. Determinants of reduced genetic capacity for butyrate synthesis by the gut microbiome in Crohn’s disease and ulcerative colitis. J. Crohn’s Colitis. 2018;12:204-216.

    Not in our library10.1093/ecco-jcc/jjx137

  176. 176.

    Magro D.O., Santos A., Guadagnini D., de Godoy F.M., Silva S.H.M., Lemos W.J.F., Vitulo N., Torriani S., Pinheiro L.V., Martinez C.A.R., et al. Remission in Crohn’s disease is accompanied by alterations in the gut microbiota and mucins production. Sci. Rep. 2019;9:53.

    Not in our library10.1038/s41598-019-49893-5

  177. 177.

    Shahir N.M., Wang J.R., Wolber E.A., Schaner M.S., Frank D.N., Ir D., Robertson C.E., Chaumont N., Sadiq T.S., Koruda M.J., et al. Crohn’s disease differentially affects region-specific composition and aerotolerance profiles of mucosally adherent bacteria. Inflamm. Bowel Dis. 2020;26:1843-1855.

    Not in our library10.1093/ibd/izaa103

  178. 178.

    Park Y.M., Ha E., Gu K.-N., Shin G.Y., Lee C.K., Kim K., Kim H.J. Host genetic and gut microbial signatures in familial inflammatory bowel disease. Clin. Transl. Gastroenterol. 2020;11:e00213.

    Not in our library10.14309/ctg.0000000000000213

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