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

Abstract

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.