Effects of different Helicobacter pylori phenotype on gastric mucosal pathogenesis

Objective:To explore the effects of different Helicobacter pylori (Hp) phenotype on expression of ki-67 in gastric mucosa. Methods:137 patients (with Hp infection) with chronic gastritis(CG), peptic ulcer or gastric cancer and 34 patients without Hp infection were observed. All patients with gastroduodenal diseases were diagnosed by endoscopy and histology. Western blotting was used to detect phenotypes of Hp Cytotoxin-associated protein (CagA), vacuolating cytotoxin (VacA), Urease and their sub-phenotypes. In Hp associated gastritis, histological grade of chronic inflammation (CI), polymorphonuclear neutrophil activity(PA) and density of Hp (DH) were scored according to the Updated Sydney System. Immunohistochemistry was used to exam the expression of ki-67. Results:①Expression rates of Hp128000CagA, 116000CagA, 95000VacA, 91000VacA and 30000UreA in the group of mild grade of CI were lower than those in the moderate-marked group (P0.05,respectively); Hp infection rate and expression rates of 95000VacA, 91000VacA and 30000UreA in the group of mild grade of PA were lower than those in the moderate-marked group (P0.05,respectively).②ki-67LI in Hp(+) CG group were higher than that of Hp(-) CG group (P=0.041). In Hp(+) CG, ki-67LI in the group of moderate-marked grade of DH was higher than that in the mild grade of CI group (P=(0.014).) In Hp(+) CG, ki-67LI in the group of moderate-marked grade of CI was higher than that in the mild grade of CI group (P=0.039), while no significances were found in Hp(-) CG group (P(0.05,)respectively).③In Hp(+) CG, (ki-67LI) in the group with expression of (128000)CagA, 95000VacA or 30000UreA were higher than that in groups without their expression. In Hp(+) gastric cancer, (ki-67LI) in the group with expression of 128000CagA was higher than that in the group without its expression((P=)0.02). Conclusion:Many virulent factors of Hp may cause increased grade of CI and play an important role in the occurrence and development of PA. Hp infection and density of Hp seem to cause increased epithelial cell proliferation in gastric mucosa with chronic gastritis. But they may exert different influences on malignant and benign gastric mucosa, and more virulent factors probably increase epithelial cell proliferation in gastric mucosa with chronic gastritis rather than gastric cancer.