| Objectives: To evaluate the characteristic of Helicobacter pylori (H. pylori) phenotypes in Nanchang area and study the relationship between H. pylori or its phenotypes and gastroduodenal diseases or the expression of ki-67 and p53 in gastric mucosa, and expolre the effect of many virulent factors of H. pylori on gatric mucosal pathogenesis.Methods: Of 288 sujects (from Nanchang area) with or without H. pylori infection, 254 sujects with H. pylori infection included 36 volunteers without gastroduodenal symptoms and 218 patients with chronic gastritis, peptic ulcer or gastric cancer. 34 patients without H. pylori infection were involved. All patients with gastroduodenal diseases were diagnosed by endoscopy and histology. Western blotting was used to detect phenotypes of H. pylori Cytotoxin-associated protein (CagA), vacuolating cytotoxin (VacA), Urease, Flagellin and their sub-phenotypes. In this study, H. pylori status was assessed according to the criterion made by Chinese Medical Association. In H. pylori associated gastritis, histological grade of chronic inflammation, polymorphonuclear neutrophil acativity and density of H. pylori were scored according to the Updated Sydney System. Immunohistochemistry was used to exam the expression of ki-67 and p53 antigen. Epithelial cell proliferation and overexpression of p53 protein were determined by means of ki-67 labelling index and p53 H-score respectively.Results: â‘ In this general population with H. pylori infection, the total expression rate of CagA, VacA, Urease and Flagellin is 57.1%, 78.6%, 100%, 95.7%, respectively. No significant relationship between any single specific phenotype and clinical outcomes was found (p>0.05). â‘¡Both ki-67LI and p53Hscore in H. pylori positive CG group are higher than those of H. pylori negative CG group (p=0.041,p=0.002, respectively). In H. pylori positive CG, both ki-67LI and p53Hscore in group of moderate-marked grade of CI are higher than those of mild group (p<0.05), while no significances were found in H. pylori negative CG group (p>0.05). In H. pylori positive CG, ki-67LI in group of moderate-marked grade of DH is higher than that of mild group (p<0.05); no significance between two groups was found (p>0.05). â‘¢H. pylori infection rate and expression rates of 128KDCagA, 116KDCagA, 95KDVacA, 91KDVacA and 30KDUreA in group of mild grade of CI are lower than those of moderate-marked group (p<0.05); H. pylori infection rate and expression rates of 95KDVacA, 91KDVacA and 30KDUreA in group of mild grade of PA are lower than those in moderate-marked group (p<0.05). â‘£In H. pylori positive CG, ki-67LI in group with expression of 128KDCagA, 95KDVacA or 30KDUreA are higher than those in group without expression. In H. pylori positive gastric cancer, ki-67LI in group with expression of 128KDCagA is higher than that in group without expression (p<0.05). No significant relationship between any single specific phenotype and p53Hscore in CG or gastric cancer was found (p>0.05).Conclusions: â‘ In Nanchang area, the total expression rate of CagA in the population with H. pylori infection is obviously lower than that of VacA. My results differ from previous reports from other regions. This may reflect differences of race and geography. â‘¡H. pylori infection and density of H. pylori seems to cause increased Epithelial cell proliferation in gastric mucosa, H. pylori infection may cause increased overexpression of p53, whereas density of H. pylori isn't related to p53 overexpression. â‘¢128KDCagA, 116KDCagA, 95KDVacA, 91KDVacA and 30KDUreA may cause increased grade of CI, and 95KDVacA, 91KDVacA and 30KDUreA may play an important role on occurrence and development of PA. â‘£ In H. pylori associated CG, 128KDCagA, 95KDVacA and 30KDUreA seem to cause increased epithelial cell proliferation in mucosa of gastritis. 128KDCagA is associated with proliferation of gastric cancer. This suggests that 128KDCagA may cause increased proliferation in mucosa of gastric cancer. H. pylori infection is associated with overexpression of p53,... |
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