IL-17 is a protection effector against the adherent-invasive Escherichia coli in murine colitis. (January 2018)

• Record Type: Journal Article
• Authors: Zhang, Hai-jia; Xu, Bin; Wang, Hu; Xu, Bing; Wang, Guo-dong; Jiang, Ming-zuo; Lei, Chao; Ding, Mei-ling; Yu, Peng-fei; Nie, Yong-zhan; Wu, Kai-chun; Sha, Su-mei; Li, Meng-bin
• Is Part Of: Molecular immunology. Volume 93(2018:Jan.)
• Page Start: 166
• Page End: 172
• Publication Date: 2018-01
• Subjects: CD Crohn's disease -- UC ulcerative colitis -- IBD inflammatory bowel disease -- AIEC adherent invasive Escherichia coli -- RT-PCR reverse transcriptase polymerase chain reaction -- DSS dextran sodium sulfate -- TEM transmission electron microscope -- SEM Scanning electron microscopy; IL-17 -- IL-22 -- IBD -- AIEC; Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2017.11.020
• Languages: English
• ISSNs: 0161-5890

Abstract

Highlights: IL-17 is essential in host defense against extracellular pathogens at mucosal sites. IL-17 deficiency exacerbates (aggravates) colitis in AIEC + DSS model. IL-17 alleviates mucosa damage in AIEC + DSS model by promoting IL-22 production. We provide a better understanding of the pathogenesis of IBD by relating the aberrant immune response and gut commensal microbes. Abstract: Inflammatory bowel disease (IBD) is caused by aberrant immune responses to the gut microbiota. Among the gut microbiota, adherent-invasive Escherichia Coli (AIEC) is thought to be the pathogen through invading the intestinal epithelial cells and causing inflammation. IL-17 secretion increase, induced by enhanced bacterial adhesion to the intestine epithelium, could on one hand protect the mucosa, but on the other hand, over amount of IL-17 initializes inflammation reactions that in turn damages the mucosa. The relationship between IL-17 and AIEC is still unclear. In this study, we tried to elucidate the function of IL-17 in AIEC-mediated colitis. Wild type (WT) and IL-17 knockout (IL-17 KO) mice were inoculated with AIEC strain E. coli LF82 and treated with dextran sodium sulphate (DSS). Histological examination of the colon was performed. Mucosa damage was assessed and scored. IL-22 and IL-17 in colon tissues were detected by ELISA, qPCR and immunohistochemistry methods. Transient AIEC colonization in IL-17 KO mice resulted in increased intestinal epithelial damage, systemic bacterial burden and mortality compared with WT controls. Moreover, IL-17 is required for the induction of IL-22 in the experimental animal models during AIEC strain E. coli LF82 colonization. These results indicate IL-17 plays a protective role in AIEC strain E. coli LF82 induced colitis by promoting IL-22 secretion.