MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice

Namiko Hoshi, Dominik Schenten, Simone A. Nish, Zenta Walther, Nicola Gagliani, Richard A. Flavell, Boris Reizis, Zeli Shen, James G. Fox, Akiko Iwasaki and Ruslan Medzhitov ()
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Namiko Hoshi: Yale University School of Medicine
Dominik Schenten: Yale University School of Medicine
Simone A. Nish: Yale University School of Medicine
Zenta Walther: Yale University School of Medicine
Nicola Gagliani: Yale University School of Medicine
Richard A. Flavell: Yale University School of Medicine
Boris Reizis: Columbia University Medical Center
Zeli Shen: Massachusetts Institute of Technology
James G. Fox: Massachusetts Institute of Technology
Akiko Iwasaki: Yale University School of Medicine
Ruslan Medzhitov: Yale University School of Medicine

Nature Communications, 2012, vol. 3, issue 1, 1-10

Abstract: Abstract Commensal bacterial sensing by Toll-like receptors is critical for maintaining intestinal homeostasis, but can lead to colitis in the absence of interleukin-10. Although Toll-like receptors are expressed in multiple cell types in the colon, the cell type(s) responsible for the development of colitis are currently unknown. Here we generated mice that are selectively deficient in MyD88 in various cellular compartments in an interleukin-10−/− setting. Although epithelial expression of MyD88 was dispensable, MyD88 expression in the mononuclear phagocyte compartment was required for colitis development. Specifically, phenotypically distinct populations of colonic mononuclear phagocytes expressed high levels of interleukin-1β, interleukin-23 and interleukin-6, and promoted T-helper 17 responses in the absence of interleukin-10. Thus, gut bacterial sensing through MyD88 in mononuclear phagocytes drives inflammatory bowel disease when unopposed by interleukin-10.

Date: 2012
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DOI: 10.1038/ncomms2113

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