Microbiota_of_Il22ra1_deficient_mice_1-sc-2013-03-25T15:15:20Z-2577
Microbiota_of_Il22ra1_deficient_mice_1
This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/  Interleukin-22 is a cytokine secreted by immune cells within gastrointestinal tract. Its receptor, encoded by the IL22ra1 gene, is specifically expressed by epithelial cells and mediates the production of antimicrobial and anti-apoptotic factors to enhance the host barrier function. Deficiency in IL-22 signalling has been linked to infectious and inflammatory conditions of the skin and gut. However, the role of its receptor in intestinal homeostasis has not been studied. Using a novel IL22ra1 knockout mouse developed at Sanger, we have shown that IL22ra1 deficiency renders mice susceptible to bacterial pathogens, including Citrobacter rodentium and Clostrium difficile. These mice have reduced levels of antimicrobial factors, as well as abnormal myeloid and T cell populations in the colon. Our findings suggest that in the absence of IL22ra1, the intestinal microbia may be perturbed, leading to loss of colonization resistance and susceptibility to pathogens.
This study aims to address the hypothesis that defective IL-22 signaling alters the intestinal microbiota in IL22ra1-knockout mice during infection with Citrobacter rodentium. To follow changes of the gut microbial populations during infection, we obtained faecal pellets from individual IL22ra1 knockout and wildtype mice before C. rodentium inoculation, and at day 3 and 8 post-infection. At day 9, their caecal contents were also obtained. Overall this experiment will allow us to determine specific bacterial populations that emerge in the absence of IL-22-dependent factors, during enteric infection.