The Toll-like receptor adaptor protein MyD88 is essential for the regulation of intestinal homeostasis in mammals.
In this study, we determined that Myd88-deficient mice are susceptible to colonic damage that is induced by dextran sulfate sodium (DSS) administration resulting from uncontrolled dissemination of intestinal commensal bacteria.
The DSS-induced mortality of Myd88-deficient mice was completely prevented by antibiotic treatment to deplete commensal bacteria.
By using cell type-specific Myd88-deficient mice, we established that B cell-intrinsic MyD88 signaling plays a central role in the resistance to DSS-induced colonic damage via the production of IgM and complement-mediated control of intestinal bacteria.
Our results indicate that the lack of intact MyD88 signaling in B cells, coupled with impaired epithelial integrity, enables commensal bacteria to function as highly pathogenic organisms, causing rapid host death.
2012-02-27
Eng.
Department of Immunology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.
Immunity. 2012 Feb;36(2):228-38
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