IL-22 is an important cytokine at barrier surfaces that triggers the production of antimicrobial peptides and mucus. Flavell and colleagues in the Journal of Immunology use an IL-22-deficient mouse to demonstrate that this cytokine shapes the population of colonic microbes to prevent colitogenicity. IL-22-deficient mice have ostensibly normal colonic morphology and do not manifest spontaneous inflammation; however, induced colitis is worse in those mice than in wild-type mice. Furthermore, wild-type mice cohoused with IL-22-deficient mice have more severe induced colitis, which suggests that the colitis is transmissible. Pyrosequencing indicates that the microbial phyla in IL-22-deficient mice differs from that of wild-type mice and, more notably, the microbiota of wild-type mice cohoused with IL-22-deficient mice more closely resembles that of the IL-22-deficient mice. As expected, IL-22-deficient mice have a lower abundance of the antimicrobial peptides RegIIIβ and RegIIIγ but, curiously, so do wild-type mice cohoused with those mice. This suggests that the microbiota is both shaped by IL-22 and, in turn, also influences its expression.

J. Immunol. (12 April 2013) doi:10.4049/jimmunol.1300016