Helicobacter pylori dwelling on the apical surface of gastrointestinal epithelium damages the mucosal barrier through direct contact.

Abstract

Epithelial junctions and mucins compose a major portion of the mucosal barrier. Helicobacter pylori (H. pylori) infections induce alterations of the tight junctions and adherens junctions in epithelial cells, although the precise mechanisms underlying this process are not fully understood. The expression of adhesion molecules and MUC1 was systematically investigated in gastrointestinal epithelial cells infected with H. pylori in vitro and in vivo. Furthermore, we developed several new in vitro methods to study the relationships between the bacterium and the dysfunction of tight junctions using Boyden Chambers. The expression of a series of junctional molecules and MUC1 decreased in the cultured cells that were infected with H. pylori. According to the degree of damage at the tight junctions, direct contact of H. pylori with the apical membrane of the cells resulted in the greatest increase in permeability compared to basal membrane binding or non-binding of H. pylori to the cells. Similarly, we noted that H. pylori infection could reduce the expression and glycosylation of MUC1. Helicobacter pylori dwelling on the apical surface of the gastrointestinal epithelium could directly induce serious injury of the mucosal barrier, and the new methods outlined here, based on the Boyden Chamber system, could be very useful for studying the relationships between bacteria and their target cells.