The role of TLR2 in the host response to pneumococcal pneumonia in absence of the spleen

<p>Abstract</p> <p>Background</p> <p>Asplenic individuals are susceptible for overwhelming infection with <it>Streptococcus pneumoniae</it>, carrying a high mortality. Although Toll-like receptor (TLR)-2 is considered the major receptor for Gram-positive bacteria in innate immunity, it does not play a major role in host defense against pneumococcal pneumonia. We wanted to investigate if in absence of an intact spleen as a first line of defense, the role of TLR2 during pneumococcal pneumonia becomes more significant, thereby explaining its insignificant role during infections in immune competent hosts.</p> <p>Methods</p> <p>We intranasally infected splenectomized wildtype (WT), TLR2 knock-out (KO) and TLR2/4 double KO mice with either serotype 2 or 3 <it>S. pneumoniae</it>.</p> <p>Results</p> <p>There were no differences between asplenic WT and TLR2KO mice of bacterial loads in lung homogenates and blood, cytokine and chemokine levels in the lungs, and lung pathology scores. TLR2/4 double KO mice were not impaired in bacterial control as well, which indicates that besides the interaction between <it>S. pneumoniae</it> and TLR2, the interaction between pneumolysin and TLR4 does not stimulate antibacterial defense in the asplenic host either.</p> <p>Conclusions</p> <p>These results argue against a significant role of TLR2 in host defense during <it>S. pneumoniae</it> pneumonia in the asplenic state. Therefore, other components can provide sufficient backup mechanisms for TLR2 deficiency in the defense against intrapulmonary infections with <it>S. pneumoniae</it> of the otherwise immune competent host.</p>

Abstract licence: CC BY-NC-ND

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