Lipopolysaccharide Regulation of Intestinal Tight Junction Permeability Is Mediated by TLR4 Signal Transduction Pathway Activation of FAK and MyD88.

ABSTRACT: Gut-derived bacterial LPS plays an essential role in inducing intestinal and systemic inflammatory responses and have been implicated as a pathogenic factor in necrotizing enterocolitis and inflammatory bowel disease. The defective intestinal tight junction barrier was shown to be an important factor contributing to the development of intestinal inflammation. LPS, at physiological concentrations, causes an increase in intestinal tight junction permeability (TJP) via a TLR4-dependent process; however, the intracellular mechanisms that mediate LPS regulation of intestinal TJP remain unclear. The aim of this study was to investigate the adaptor proteins and the signaling interactions that mediate LPS modulation of intestinal tight junction barrier using in vitro and in vivo model systems. LPS

SUBMITTER: Guo S 

PROVIDER: S-EPMC4637237 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature