Differential E-cadherin expression in helicobacter-related gastric pathology

Background and aims E-cadherin plays an important role in the maintenance of cell–cell adhesion. Loss of E-cadherin expression is fundamental in the development of many epithelial malignancies. Helicobacter pylori (H. pylori) is an important etiological factor in the development of many gastric diseases, including gastritis, peptic ulcer disease, and gastric carcinoma. In this study, we related different histopathological findings to the absence and presence of helicobacter infection, and investigated E-cadherin expression in H. pylori-negative and H. pylori-positive gastritis. This study aimed to find the prevalence of H. pylori colonization in chronic gastritis patients and its association with different histomorphological changes of chronic gastritis. Also, we aimed to evaluate E-cadherin expression in chronic gastritis as a prestage in the development of gastric carcinoma, and its relation to H. pylori. Materials and methods In total, 40 cases of gastritis samples were obtained by endoscopy; hematoxylin and eosin staining, Giemsa stain, and E-cadherin immunostain were done; we related different histopathological findings to the absence and presence of helicobacter infection. Also, we reported the changes in E-cadherin expression in relation to histopathological findings of chronic gastritis, and investigated E-cadherin expression in H. pylori-negative and H. pylori-positive gastritis. Results H. pylori was seen in 62.5% of cases. There was a statistically significant correlation between the presence of H. pylori and increase of the severity of chronic inflammation, neutrophilic activity, and presence of glandular atrophy (P=0.05, 0.003, and 0.04), respectively. Also, there was a significant decrease in E-cadherin expression with the increase in the severity of chronic inflammation, neutrophilic activity, and presence of glandular atrophy (P=0.04, 0.05, and 0.03), respectively. A statistically significant correlation between the presence of H. pylori and decrease in E-cadherin expression was found (P=0.01). Conclusion In chronic gastritis, there is high prevalence of H. pylori infection and decrease in E-cadherin expression. Also, there is an increase in the severity of chronic gastritis with the increase in the prevalence of H. pylori and this is associated with a decrease in E-cadherin expression, which precedes gastric carcinoma.