[Relationship between Helicobacter pylori infection and proliferation and apoptosis of gastric epithelial dysplasia cell]

Abstract

Background & objective: Gastric epithelial dysplasia is the precancerous lesion of gastric cancer. However, the mechanism that dysplasia evolves to malignancy is not clear. In order to clarify the relationship between Helicobacter pylori (HP) infection and its virulence factor and changes of cell kinetics of dysplasia, the authors measured the changes of proliferation and apoptosis and the status of HP infection.

Methods: A total of 117 gastric mucosal biopsy specimens were enrolled, including 12 of chronic superficial gastritis (CSG) and 105 of dysplasia. Dysplasia samples were divided into two groups: 35 of high-grade dysplasia [carcinogenesis group (n=30), regression group (n=5)], 70 of low-grade dysplasia [carcinogenesis group (n=18), regression group (n=52)]. The expression of proliferating cell nuclear antigen (PCNA) was measured by immunohistochemical staining; cell apoptosis was determined by terminal deoxynucleotidyl transferase mediated nick end labeling(TUNEL); the status of HP infection was detected by polymerase chain reaction(PCR) with specific primers of urea A and cagA gene.

Results: There was no significant difference of HP infection between dysplasia and CSG(84.76% vs. 83.33%), but CagA-positive strain infection rate in dysplasia was slightly higher than that in CSG (85.39% vs. 60.00%). Proliferation indexes(PI) in the patients with HP infection and CagA(+) strain infection were higher than that in the patients without HP infection and CagA(-)strain, respectively (P< 0.05). PI was positively associated with the status of HP and CagA(+) strains infection (P< 0.05). AI/PI ratio (AI: apoptosis index) was negatively associated with CagA-positive strain infection (P< 0.05).

Conclusion: Gastric epithelial dysplasia cells have abnormal changes in PI and AI when it evolves to malignancy, and the abnormal cell kinetics is partly correlated with HP and CagA(+) strain infection. So treatment of HP infection may produce a good result for the evolution of dysplasia.