Alterations in gastric mucin synthesis by Helicobacter pylori

Abstract

AIM: To determine the role of Helicobacter pylori in altering gastric mucin synthesis and define how this process relates to H. pylori-related diseases.

METHODS: Analyses of human gastric tissues using immunohistochemistry and in situ hybridization document the role of H. pylori in altering the composition and distribution of gastric mucins.

RESULTS: These data indicate a decrease in the product of the MUC5 (MUC5AC) gene and aberrant expression of MUC6 in the surf ace epithelium of H. pylori-infected patients. A normal pattern was restored by H. pylori eradication. Inhibition of mucin synthesis including MUC5AC and MUC1 mucins by H. pylori has been established in vitro using biochemical and Western blot analyses. This effect is not due to inhibition of glycosylation, but results from inhibition of synthesis of mucin core structures. In vitro experiments using inhibitors of mucin synthesis indicate that cell surface mucins decrease adhesion of H. pylori to gastric epithelial cells.

CONCLUSION: Inhibition of mucin synthesis by H. pylori in vivo can disrupt the protective mucous layer and facilitate bacterial adhesion, which may lead to increased inflammation in the gastric epithelium.

Key Words: Mucins, Glycoproteins, Gastric mucin/biosynthesis, Gastric mucosa, Helicobacter pylori, Glycosylation, In vitro, Immunohistochemistry, In situ hybridization