Intestinal epithelial barrier damage is closely related to a variety of gastrointestinal disease, how to maintain its function effectively is the key to treat all these diseases.This research attempts to explore the protective effect and its mechanism of toll-like receptor 2(Toll -like receptor, TLR2)on permeability of intestinal epithelial barrier by experiments in vitro, to lay a foundation for new treatment methods.

We cultured non-transfected Caco-2 cells, TLR2-deficiency Caco-2 cells, TLR2-overexpressed Caco-2 cells in normal control group until the 21st d, then tested transepithelial electrical resistance(TEER)which reacts the permeability of epithelial barrier.We cultured 3 types of cells in inflammation group until the 19th d treated with 10 ng/ml IL-1 beta for 48 h, then tested TEER values at the 21st d. We treated 3 types of cells in inhibition group with PI3K/Akt pathway inhibitor for 1h befor IL-1 beta, then tested TEER values at the 21st d.

TEER value of TLR2-deficiency Caco-2 cell monolayer significantly reduced(P<0.01), whereas TEER value of TLR2-overexpressed Caco-2 monolayer raised, but without statistically significant.TLR2 can prevent IL-1 beta caused TEER decreasing(P<0.01), but the effect disappeared after given PI3K/Akt pathway inhibitor.

TLR2 can regulate the permeability of intestinal epithelial barrier.In addition, TLR2 can protect permeability increasing caused by inflammation, this effect mediated by PI3K/Akt pathway.

Intestinal epithelial barrier; Transepithelial electrical resistance; TLR2; PI3K/Akt pathway; Inflammatory bowel disease