Relation between gastric epithelial cell proliferation and expression of CagA and VacA in Helicobacter pylori infection.
- Author:
Nam Il KIM
1
;
Jung Hyun LEE
;
Yeoung Sil LEE
;
Jae Uk LEE
;
Goo LEE
;
Jeong Ill SUH
;
Chang Heon YANG
;
Chang Woo LEE
;
Hwan Jung YUN
;
Tae Jung JANG
;
Jung Ran KIM
;
Gyoung Yim HA
Author Information
1. Department of Internal Medicine, Dongguk University College of Medicine, Kyongju, Korea.
- Publication Type:Original Article
- Keywords:
Helicobacter pylori;
CagA;
VagA;
Gastric epithelial proliferation
- MeSH:
Antibodies;
Atrophy;
Biopsy;
Cell Proliferation;
Duodenal Ulcer;
Endoscopy, Digestive System;
Epithelial Cells*;
Gastritis;
Helicobacter pylori*;
Helicobacter*;
Humans;
Immunoglobulin G;
Inflammation;
Metaplasia;
Stomach Neoplasms;
Stomach Ulcer
- From:Korean Journal of Medicine
2000;58(5):516-525
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Infection with Helicobacter pylori (H. pylori) has been associated with an increased risk for developing gastric cancer. This risk is further enhanced with CagA positive H. pylori strains. Increased epithelial cell proliferation is associated with an increased risk for gastric cancer. The aim of the study was to investigate whether the gastric epithelial cell proliferation was related to the expression of CagA and VacA in H. pylori infection. METHODS: The subjects were 77 patients who had undergone diagnostic esophagogastroduodenoscopy with biopsy; 18 gastritis, 18 gastric ulcer, 17 duodenal ulcer and 24 gastric cancer. The expression of cytotoxic genes was determined indirectly by assaying serum IgG antibodies to specific antigens of H. pylori. Gastric epithelial cell proliferation was assessed using immunohistochemical method using Ki-67 monoclonal antibody. Acute and chronic inflammation, intestinal metaplasia and glandular atrophy were scored according to the updated Sydney system. RESULTS: Ki-67 labeling index, acute and chronic inflammation were significantly higher in H. pylori infected persons (n=70, 90.9%) than in uninfected persons (n=7, 9.1%) (p< 0.05), but the difference in intestinal metaplasia and glandular atrophy between the two groups was not statistically significant. Ki-67 labeling indices in persons infected with CagA positive strains (n=56, 80.0%) were significantly higher than in persons infected with CagA negative strains (n=14, 20%) (0.55+/-0.13 vs 0.37+/-0.17, p< 0.05), but the differences in acute and chronic inflammation, intestinal metaplasia and glandular atrophy between the two groups were not statistically significant. No significant difference was found in Ki-67 labeling index, acute and chronic inflammation, intestinal metaplasia and glandular atrophy according to expression of VacA. CONCLUSION: Gastric mucosal cell proliferation, which might be closely involved in the pathogenesis of gastric carcinoma, was significantly higher in CagA positive H. pylori infected persons.
