Host Gene Expression and Virulence factor of Helicobacter pylori in patients with Chronic Gastritis

Abstract

Chronic gastritis an inflammation of the mucosal layer of the stomach is a major clinical entity due to its association with gastrointestinal disorders Chronic bacterial infection of the stomach by Helicobacter pylori H pylori is the most common causes of this disorder The H pylori is a spiral shaped microaerophilic flagellated gram negative bacterium infecting around half the worlds population whose major reservoir is the human stomach Although H pylori do not cause illness in most infected people it is the major causative agent of chronic active gastritis and an important etiological factor in the pathogenesis of peptic ulcer disease and gastric cancer Moreover the pathogenesis of gastric disorders and the pathogenic effect is shown to be associated with host bacterial interplay Chronic gastritis is implicated as the early step during the development of gastric cancer which can break through chronic atrophic gastritis multifocal atrophic gastritis intestinal metaplasia dysplasia and invasive carcinoma A variety of oncogenic pathways are triggered by H pylori in epithelial cells leading to epithelial cell proliferation and differentiation altered apoptosis rate increased inflammatory cytokine production that results in epithelial cell oncogenic transformation Hence identification of host genetic determinant that inclined to the disease condition driven by H pylori provide insights to reveal the carcinogenic mechanisms that contribute to the understanding of the pathogenesis of gastric diseases The present study emphasizes the significance of H pylori virulent genes and host gene expression in the pathogenesis of gastric diseases Initial screening methods to detect the presence of H pylori by RUT histopathology urease test and ELISA showed that the percentage of detection varies from 36 percent to 58 percent and the sensitivity of test methods showed a higher statistical significance The expression levels of H pylori virulent genes CagA VacA and UreA and host genes catenin CCL20 actin CXCR4 and CD69 in patients