Detection of virulence marker of H. pylori, sabA gene and analysis of expression and characterization of polymorphisms -238 and -850 of tumor necrosis factor gene in gastric inflammatory process

• Grant number: 16/14449-8
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): October 01, 2016
• Effective date (End): September 30, 2017
• Field of knowledge: Biological Sciences - Genetics - Human and Medical Genetics
• Principal Investigator: Lucas Trevizani Rasmussen
• Grantee: Jéssica Nunes Pereira
• Host Institution: Pró-Reitoria de Pesquisa e Pós-Graduação. Universidade do Sagrado Coração (USC). Bauru , SP, Brazil

Abstract

The Tumor Necrosis Factor is a proinflammatory cytokine, mainly synthesized by macrophages and monocytes, and is the main stimulus for the production thereof, the lipopolysaccharides that are the membrane of Gram-negative bacteria. The Helicobacter pylori is a gram-negative bacterium that colonizes the mucosa of the stomach and is responsible for various gastroduodenal diseases such as gastritis, ulcers, and gastric cancer appears to induce the production of TNF-±, which acts as a potent inhibitor of secretion gastric, contributing to the development of peptic diseases, and is the most powerful mediator of the inflammatory response against gram-negative bacteria. In view of TNF-± involvement and the presence of H. pylori in the development of gastric diseases, this project aims to characterize the polymorphisms of the promoter region -850 (rs1799724) and -238 (rs361525) of TNF-± by PCR -RFLP to detect the pathogenicity of H. pylori marker, sabA gene and analyze gene expression by Real-time PCR of TNF-± gene in 150 samples from gastric biopsies of patients with peptic and gastric cancer symptoms, with an order to associate genotypes found to TNF-± expression and correlate them the presence of H. pylori and its main pathogenic markers. The development of this approach may open new perspectives for the characterization of factors involved in peptic diseases and gene regulation, aimed at a better understanding of the pathophysiological mechanisms of these diseases.