Toll-like receptor 5-deficient mice have dysregulated intestinal gene expression and nonspecific resistance to Salmonella-induced typhoid-like disease.

ABSTRACT: The recognition of flagellin by Toll-like receptor 5 (TLR5) is the dominant means by which model intestinal epithelia activate proinflammatory gene expression in response to Salmonella enterica. The role of the flagellin-TLR5 interaction in vivo has been addressed primarily via studies that use flagellar mutants. Such studies suggest that host recognition of flagellin promotes rapid neutrophil recruitment that protects the host from this pathogen. However, these works do not directly address the role of TLR5 and are subject to the caveat that flagellar mutations may broadly affect Salmonella gene expression. Thus, we examined the role of the flagellin-TLR5 interaction via the use of TLR5-deficient (TLR5KO) mice. We utilized both the traditional model of murine Salmonella infection, wherein

SUBMITTER: Vijay-Kumar M 

PROVIDER: S-EPMC2258833 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature