IL-33 promotes recovery from acute colitis by inducing miR-320 to stimulate epithelial restitution and repair.

ABSTRACT: Defective and/or delayed wound healing has been implicated in the pathogenesis of several chronic inflammatory disorders, including inflammatory bowel disease (IBD). The resolution of inflammation is particularly important in mucosal organs, such as the gut, where restoration of epithelial barrier function is critical to reestablish homeostasis with the interfacing microenvironment. Although IL-33 and its receptor ST2/ILRL1 are known to be increased and associated with IBD, studies using animal models of colitis to address the mechanism have yielded ambiguous results, suggesting both pathogenic and protective functions. Unlike those previously published studies, we focused on the functional role of IL-33/ST2 during an extended (2-wk) recovery period after initial challenge in dextran sodiu

SUBMITTER: Lopetuso LR 

PROVIDER: S-EPMC6176569 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature