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The Cytokine IL-22 Promotes Pathogen Colonization by Suppressing Related Commensal Bacteria

2014; Cell Press; Volume: 40; Issue: 2 Linguagem: Inglês

10.1016/j.immuni.2014.01.003

1097-4180

Judith Behnsen, Stefan Jellbauer, Christina P. Wong, Robert A. Edwards, Michael D. George, Wenjun Ouyang, Manuela Raffatellu,

Viral gastroenteritis research and epidemiology

Interleukin-22 (IL-22) is highly induced in response to infections with a variety of pathogens, and its main functions are considered to be tissue repair and host defense at mucosal surfaces. Here we showed that IL-22 has a unique role during infection in that its expression suppressed the intestinal microbiota and enhanced the colonization of a pathogen. IL-22 induced the expression of antimicrobial proteins, including lipocalin-2 and calprotectin, which sequester essential metal ions from microbes. Because Salmonella enterica ser. Typhimurium can overcome metal ion starvation mediated by lipocalin-2 and calprotectin via alternative pathways, IL-22 boosted its colonization of the inflamed intestine by suppressing commensal Enterobacteriaceae, which are susceptible to the antimicrobial proteins. Thus, IL-22 tipped the balance between pathogenic and commensal bacteria in favor of a pathogen. Taken together, IL-22 induction can be exploited by pathogens to suppress the growth of their closest competitors, thereby enhancing pathogen colonization of mucosal surfaces.