Effect of Helicobacter pylori eradication on proliferation and apoptosis of gastric epithelial cells.
- Author:
Goo LEE
1
;
Suk Jin CHOI
;
Young Hwan CHOI
;
Dong Gun PARK
;
Wan Da SEO
;
Jeong Il SUH
;
Chang Heon YANG
;
Chang Woo LEE
;
Tae Jung JANG
;
Jung Ran KIM
Author Information
1. Department of Internal Medicine, College of medicine, Dongguk University, Kyungju, Korea.
- Publication Type:Original Article
- Keywords:
H. pylori;
Apoptosis;
Ki-67;
Acute inflammation;
Chronic inflammation;
Intestinal metaplasia
- MeSH:
Apoptosis*;
Carcinogenesis;
Cell Proliferation;
Duodenal Ulcer;
Epithelial Cells*;
Gastritis;
Helicobacter pylori*;
Helicobacter*;
Humans;
Inflammation;
Metaplasia;
Peptic Ulcer;
Stomach Neoplasms;
Stomach Ulcer;
Transferases;
Urease
- From:Korean Journal of Medicine
1999;57(3):288-297
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Helicobacter pylori (H. pylori) is the principle cause of type B gastritis and peptic ulcer disease and has been classified as group I carcinogen for gastric cancer. H. pylori may affect the normal balance between gastric cell proliferation and epithelial cell death, thus interfering with the maintenance of gastric mucosal integrity. The aim of this study was to investigate the effect of H. pylori on cell proliferation and apoptosis according to the effect of eradication of H. pylori. METHODS: The subjects were 45 patients who had undergone diagnostic gastroduodenoscopy; 11 with gastritis, seven with gastric ulcer and 27 duodenal ulcer. H. pylori infection was assessed by H&E and immunohistochemical stain with anti-H. pylori polyclonal antibody and rapid urease test. Acute and chronic inflammation, apoptosis and intestinal metaplasia were scored according to the updated Sydney system. Gastric epithelial cell proliferation was assessed by immunohostochemical method using Ki-67 monoclonal antibody. In situ apoptosis was detected with in situ terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nick end labeling. RESULTS: Acute and chronic inflammation, intestinal metaplasia, Ki-67 labeling index, and apoptosis were significantly higher in H. pylori infected persons (n=45) than in uninfected persons (n=5)(p<0.05). Acute and chronic inflammation, intestinal metaplasia, Ki-67 labeling index and apoptosis in H. pylori eradicated group (n=25) significantly decreased after eradication therapy (p<0.05), but no significant differences of them was observed in H. pylori non-eradicated goup (n=20) after eradication therapy. Ki-67 labeling index was significantly correlated with acute inflammation, chronic inflammation and apoptosis (p<0.05). Apoptosis was significantly correlated with acute and chronic inflammation (p<0.05). CONCLUSION: In eradicated group, epithelial apoptosis and proliferation closely associated with gastric carcinogenesis are stabilized after treatment, which suggests H. pylori eradication therapymay preven the early step of gastric carcinogenesis.
