BACKGROUND: Several studies have shown that Helicobacter pylori infection is associated with enhanced gastric epithelial-cell proliferation, which is thought to be involved in its apparent carcinogenicity. This hyperproliferation is believed to be related to the inflammatory effects of the bacterium. The role of Helicobacter pylori in gastric epithelial apoptosis, however, is less clear. AIM: We attempted to identify the effect of Helicobacter pylori infection on apoptosis in the gastric epithelium and its possible relation to epithelial-cell proliferation and mucosal inflammation. PATIENTS AND METHODS: We studied cell proliferation (via bromodeoxyuridine labelling), apoptosis (using in situ TdT-mediated dUTP-biotin nick end labelling of DNA strand breaks) and mononuclear and polymorphonuclear cell infiltrates (computer-assisted image analysis) in gastric antral biopsies obtained from 37 gastritis patients (20 Helicobacter pylori-positive, 17 Helicobacter pylori-negative). RESULTS: Helicobacter pylori-positives displayed significantly enhanced proliferation within the gastric epithelium that was positively correlated with both acute and chronic inflammatory-cell densities. Apoptotic indexes were similar in both groups and showed no correlation with any of the parameters under consideration. CONCLUSIONS: Enhanced epithelial cell proliferation and an altered distribution of cycling cells within the gastric glands are a common feature of chronic superficial gastritis caused by Helicobacter pylori. In vivo immunohistochemically detected apoptosis of gastric epithelial cells does not seem to be affected by Helicobacter pylori infection. Further study is needed to clarify the effect of this infection on programmed cell death within gastric glands.
BACKGROUND: Several studies have shown that Helicobacter pylori infection is associated with enhanced gastric epithelial-cell proliferation, which is thought to be involved in its apparent carcinogenicity. This hyperproliferation is believed to be related to the inflammatory effects of the bacterium. The role of Helicobacter pylori in gastric epithelial apoptosis, however, is less clear. AIM: We attempted to identify the effect of Helicobacter pylori infection on apoptosis in the gastric epithelium and its possible relation to epithelial-cell proliferation and mucosal inflammation. PATIENTS AND METHODS: We studied cell proliferation (via bromodeoxyuridine labelling), apoptosis (using in situ TdT-mediated dUTP-biotin nick end labelling of DNA strand breaks) and mononuclear and polymorphonuclear cell infiltrates (computer-assisted image analysis) in gastric antral biopsies obtained from 37 gastritispatients (20 Helicobacter pylori-positive, 17 Helicobacter pylori-negative). RESULTS:Helicobacter pylori-positives displayed significantly enhanced proliferation within the gastric epithelium that was positively correlated with both acute and chronic inflammatory-cell densities. Apoptotic indexes were similar in both groups and showed no correlation with any of the parameters under consideration. CONCLUSIONS: Enhanced epithelial cell proliferation and an altered distribution of cycling cells within the gastric glands are a common feature of chronic superficial gastritis caused by Helicobacter pylori. In vivo immunohistochemically detected apoptosis of gastric epithelial cells does not seem to be affected by Helicobacter pylori infection. Further study is needed to clarify the effect of this infection on programmed cell death within gastric glands.
Authors: M Anti; A Armuzzi; S Morini; E Iascone; G Pignataro; C Coco; R Lorenzetti; M Paolucci; M Covino; A Gasbarrini; F Vecchio; G Gasbarrini Journal: Gut Date: 2001-02 Impact factor: 23.059