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Immunity. 2014 Feb 20;40(2):262-73. doi: 10.1016/j.immuni.2014.01.003. Epub 2014 Feb 6.

The cytokine IL-22 promotes pathogen colonization by suppressing related commensal bacteria.

Author information

1
Department of Microbiology, University of California, Irvine, Irvine, CA 92697, USA; Institute for Immunology, University of California, Irvine, Irvine, CA 92697, USA.
2
Institute for Immunology, University of California, Irvine, Irvine, CA 92697, USA; Department of Pathology and Laboratory Medicine, University of California, Irvine, Irvine, CA 92697, USA.
3
Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA 95616, USA.
4
Department of Immunology, Genentech, South San Francisco, CA 94080, USA.
5
Department of Microbiology, University of California, Irvine, Irvine, CA 92697, USA; Institute for Immunology, University of California, Irvine, Irvine, CA 92697, USA. Electronic address: manuelar@uci.edu.

Abstract

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.

Comment in

PMID:
24508234
PMCID:
PMC3964146
DOI:
10.1016/j.immuni.2014.01.003
[Indexed for MEDLINE]
Free PMC Article

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