Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges

ABSTRACT: Bacterial flagellin is a dominant innate immune activator of the intestine. Therefore, we examined the role of the intracellular flagellin receptor, NLRC4, in protecting the gut and/or driving inflammation. In accord with NLRC4 acting via transcription-independent pathways, loss of NLRC4 did not reduce the rapid robust changes in intestinal gene expression induced by flagellin administration. Loss of NLRC4 did not alter basal intestinal homeostasis nor predispose mice to development of colitis upon administration of an anti-IL-10R monoclonal antibody. However, in response to epithelial injury induced by dextran sulfate sodium (DSS), loss of NLRC4 resulted in more severe disease indicating a role for NLRC4 in protecting the gut. Moreover, loss of NLRC4 resulted in increased mortality in

ORGANISM(S): Mus musculus

SUBMITTER: Gregory Doho 

PROVIDER: E-GEOD-34492 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress