title: The cytokine IL-22 promotes pathogen colonization by suppressing related commensal bacteria.
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.
authors: Department of Microbiology, University of California, Irvine, Irvine, CA 92697, USA; Institute for Immunology, University of California, Irvine, Irvine, CA 92697, USA.
authors: Judith
authors: J
authors: Behnsen
authors: Department of Microbiology, University of California, Irvine, Irvine, CA 92697, USA; Institute for Immunology, University of California, Irvine, Irvine, CA 92697, USA.
authors: Stefan
authors: S
authors: Jellbauer
authors: Department of Microbiology, University of California, Irvine, Irvine, CA 92697, USA; Institute for Immunology, University of California, Irvine, Irvine, CA 92697, USA.
authors: Christina P
authors: CP
authors: Wong
authors: 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.
authors: Robert A
authors: RA
authors: Edwards
authors: Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA 95616, USA.
authors: Michael D
authors: MD
authors: George
authors: Department of Immunology, Genentech, South San Francisco, CA 94080, USA.
authors: Wenjun
authors: W
authors: Ouyang
authors: 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.
authors: Manuela
authors: M
authors: Raffatellu
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D054884:Host-Pathogen Interactions; D007378:Interleukins / Q000235:genetics / Q000276:immunology*; D007422:Intestines / Q000382:microbiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008954:Models, Biological; D060888:Real-Time Polymerase Chain Reaction; D012480:Salmonella Infections / Q000276:immunology* / Q000382:microbiology*; D013559:Symbiosis / Q000276:immunology*; D015854:Up-Regulation; D000097043:Interleukin-22
chemical_list: D016207:Cytokines; D007378:Interleukins; D000097043:Interleukin-22