Effects of Helicobacter pylori Infection on Apoptosis, Bcl-2 and Cell Proliferation

Bhang, Choon Sang; Choi, Myung Gyu; Kim, Jin Il; Han, Sok Won; Chung, In Sik; Park, Doo Ho; Chang, Eun Deok

Abstract

BACKGROUND/AIMS: Helicobacter pylori may promote gastric carcinogenesis mediated by the induction of gastric epithelial cell proliferation. Programmed cell death (apoptosis) is linked to cell proliferation and the bcl-2 oncogene inhibit apoptosis. The aim of this study was to assess the effects of H. pylori infection on apoptosis, Bcl-2 and gastric epithelial proliferation in chronic gastritis.
METHODS
We examined the apoptosis with in situ TdT-mediated dUTP nick end labeling and the proliferating cell nuclear antigen (PCNA) and Bcl-2 with immunohistochemical staining.
RESULTS
H. pylori-positive patients showed significantly higher apoptosis index and PCNA index (2.81+/-1.19 and 5.13+/-2.0, respectively) than negative patients (1.69+/-0.99 and 2.90+/-1.50, respectively). Successful eradication of H. pylori infection significantly reduced apoptosis and epthelial proliferation (The indices are 1.10+/-0.75 and 2.94+/-1.32). Apoptosis index was significantly related to PCNA index. Bcl-2 expression was not different between H. pylori-positive and negative patients.
CONCLUSIONS
This study suggests that H. pylori infection may increase apoptosis and epithelial proliferation, and such increases are reversed by the eradication of H. pylori.