Sean Lyons

TL;DR: Investigating how epithelia detect flagellin revealed that cell surface expression of Toll-like receptor 5 (TLR5) conferred NF-κB gene expression in response to flageLLin, providing a molecular basis for the polarity of this innate immune response.

TL;DR: It is concluded that H. pylori evades TLR5-mediated detection, which may contribute to its long-term persistence in individual hosts.

TL;DR: Toll-like receptors activate antimicrobial gene expression in response to detection of specific bacterial products, and TLR5, the only TLR thought to be preferenced by the immune system, is the first to be studied.

TL;DR: Results indicate that epithelial TLR5 mediates p38 activation and subsequently regulates flagellin-induced IL-8 expression independently of NF-kappaB, probably by influencing IL- 8 mRNA translation.

TL;DR: Apical colonization of polarized epithelia by Salmonella typhimurium results in translocation of flagellin to the basolateral membrane domain, thus enabling activation of toll-like receptor 5 (TLR5)-mediated pro-inflammatory gene expression, suggesting a role in the pathogenesis of the mucosal inflammation characteristic of human Salmonellosis.