| First Author | Behnsen J | Year | 2014 |
| Journal | Immunity | Volume | 40 |
| Issue | 2 | Pages | 262-73 |
| PubMed ID | 24508234 | Mgi Jnum | J:209929 |
| Mgi Id | MGI:5568917 | Doi | 10.1016/j.immuni.2014.01.003 |
| Citation | Behnsen J, et al. (2014) The cytokine IL-22 promotes pathogen colonization by suppressing related commensal bacteria. Immunity 40(2):262-73 |
| abstractText | 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. |
