Commensal bacterial internalization by epithelial cells: An alternative portal for gut leakiness.

摘要: Co-existing paracellular and transcellular barrier defect in intestinal epithelium was documented inflammatory bowel disease, celiac obstruction. Mechanisms regarding tight junction disruption have been extensively studied; however, limited progress has made research on bacterial transcytosis. Densely packed brush border (BB), with cholesterol-based lipid rafts the intermicrovillous membrane invagination, serves as an ultrastructural to prevent direct contact of luminal microbes cellular soma. Evidence vitro epithelial cell cultures vivo animal models obstruction antibiotic-resistant infection had indicated that nonpathogenic, noninvasive enteric bacteria may hijack raft-mediated endocytic pathways. Our studies shown low dose interferon-gamma (IFNγ) causes long myosin light chain kinase (MLCK)-dependent terminal web (TW) contraction BB fanning, allowing pass through consequently widened cleft be endocytosed via caveolin-associated rafts. Activation intracellular innate immune receptors by bacteria-containing endosomes further induce oxidative stress, leading secondary damage. The finding internalization preceding damage suggests abnormal uptake cells contribute initiation or relapse chronic inflammation.