Toll-like receptor 2-mediated intestinal injury and enteric tumor necrosis factor receptor I contribute to liver fibrosis in mice.

ABSTRACT:

Background & aims

Progression of liver fibrosis in experimental models depends on gut-derived bacterial products, but little is known about mechanisms of disruption of the mucosal barrier or translocation. We used a mouse model of cholestatic liver disease to investigate mechanisms of intestinal barrier disruption following liver injury.

Methods

Liver fibrosis and bacterial translocation were assessed in Toll-like receptor 2 (TLR2)-deficient and tumor necrosis factor receptor I (TNFRI)-deficient mice subjected to bile duct ligation. Epithelial and lamina propria cells were isolated and analyzed by immunoblot analyses and flow cytometry. We analyzed bone marrow chimeras and mice with a conditional gain-of-function allele for the TNFRI receptor. By crossing TNFRI(flxneo/flxneo

SUBMITTER: Hartmann P 

PROVIDER: S-EPMC3482543 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature