Helicobacter pylori Virulent Genes in the Upregulation of CCL20 and β-actin Expression and Progression towards Gastric Disorders

Abstract

Objectives: Helicobacter pylori , infection carryout a substantial role in the pathogenesis of gastric disorders. The pathogenic effect is shown to be associated with host bacterial interplay and Vac A and Cag A are recognized as imperative virulence determinants. A variety of carcinogenic pathways are triggered by H. pylori and CCL20 and β-actin are responsible for cellular progress and upregulation of these genes leads to metaplasia, dysplasia and gastric adenocarcinoma. Therefore, it is of interest to investigate the association of Cag A , Vac A in the upregulation of CCL20 and β-actin expression and progression towards gastric disorders. Methods : Blood and gastric biopsy samples of chronic gastritis subjects (n=100) were collected to identify the incidence of H. pylori by ELISA and Rapid urease test. The samples positive for both RUT and ELISA were subjected to RT-PCR for expression studies. Results: Among the study subjects, 36% and 58% showed positive result for RUT and ELISA of which 29% (p=0.0005) showed positive result for both RUT and ELISA. For expression studies, 48% and 90% showed higher significant (p=0.0005) expression levels of Cag A and Vac A m2. 10% (p=0.023) showed a significant expression levels of Vac A m1 region. Likewise 31% and 90% (p=0.0005) of patients showed higher significant expression levels of CCL20 and β-actin . Conclusion: Thus obtained results illustrated that H. pylori excites the production of Cag A , Vac A , CCL20 and β-actin and expression of these factors signify a promising biomarker in the early diagnosis of the infection and in analyzing the progression towards gastric disorders. J Microbiol Infect Dis 2019; 9(3):116-124.