Analysis of Interleukin-17B Gene Expression and Receptor associated with the Detection of H. pylori and the Virulence Markers, CagA and VacA genes.

Abstract

Helicobacter pylori is a microaerophilic, Gram-negative, flagellated, and spiral-shaped bacterium widely associated with gastric pathologies by creating an environment of chronic inflammation in the stomach lining. Its asymptomatic infection hinders early diagnosis and allows the progression of clinical complications. The stimulation of an exacerbated immune response disrupts cellular homeostasis through the production of cytokines (including IL-17B), leading to epithelial changes in the host, which promote apoptosis and cellular proliferation. The virulence factors CagA and VacA play a crucial role in the pathogenesis of H. pylori infection: CagA induces cell proliferation and inflammation of gastric tissue, while VacA contributes to the persistence of bacterial infection through direct tissue damage. Thus, this study aims to characterize the CagA and VacA genes in H. pylori strains isolated from gastric biopsies, correlating them with the expression of Interleukin 17B (IL-17B) and its receptor IL-17RB, investigating genetic polymorphisms, and the interaction between these inflammatory markers and histopathological findings of gastritis and gastric cancer. The research encompasses 200 gastric biopsy samples from patients, distributed into three groups: control, chronic gastritis, and gastric cancer. Detection of the bacteria, their virulence markers, IL-17B, and its receptor IL-17RB will be carried out using quantitative real-time PCR (q-PCR). The results of this study are expected to contribute to the understanding of H. pylori-induced carcinogenesis mechanisms, providing data that can be used in the development of more effective strategies for the diagnosis, prognosis, and treatment of gastric pathologies associated with this infection.