Abstracts Open Access
Copyright ©The Author(s) 2000. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 2000; 6(Suppl3): 20-20
Published online Sep 15, 2000. doi: 10.3748/wjg.v6.iSuppl3.20
Alterations in gastric mucin synthesis by Helicobacter pylori
James C Byrd, Robert S Bresalier, Gastrointestinal Cancer Research Laboratory, Henry Ford Health Sciences Center, Detroit MI 48202, United States
Robert S Bresalier, Department of Medicine, University of Michigan School of Medicine, Ann Arbor, MI, United States
Author contributions: All authors contributed equally to the work.
Supported by the Research Service of the Henry Ford Health Sciences Center and Research Foundation (JCB, RSB) and National Cancer Institute, Grant R01 CA69480 (RSB)
Correspondence to: Robert S Bresalier, MD, Gastrointestinal Cancer Research Laboratory, Henry Ford Health Sciences Center, 2799 West Grand Blvd., Detroit MI 48202, United States
Telephone: 313-916-046 Fax: 313-9169487
Received: May 12, 2000
Revised: June 28, 2000
Accepted: July 10, 2000
Published online: September 15, 2000

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

Footnotes

E- Editor: Hu S

$[References]