The role of the CagA gene in the occurrence of the inflammatory response of the gastric mucosa in patients with chronic Helicobacter pylori-associated gastritis

Abstract

Currently, Helicobacter pylori infection (H. pylori) is recognized as one of the most important risk factors for gastrocarcinogenesis. It is known that this infection does not directly cause neoplastic changes in the gastric mucosa, and this is due to a number of consecutive events due to the long persistence of the pathogen in the human body. The initial stage of this cascade, of course, is the inflammatory response, due to the body’s ability to adapt to extraneous infection, which is the inevitable result of the interaction of H. pylori with cells of the gastric epithelium. This direct damaging effect is enhanced by the production of vacuolating cytotoxin and the release of products of the cytotoxin-associated CagA gene, which, at a pathomorphological level, is manifested by inflammatory infiltration of the gastric mucosa (GM) to some extent. On the relationship between the degree of contamination and the activity of the inflammation of the GM in people infected with the CagA strain, today there are different, often conflicting opinions, which is why in this work we set the goal of establishing the relationship between the nature of the inflammatory response and the presence of the CagA gene in H. pylori- infected patients. The purpose of the study is to determinate the relationship between the nature of the inflammatory response and the genetic features of the H. pylori strain (CagA genotype).We examined 365 patients, among whom 40 people were included in the control group (18 women and 22 men, whose average age was 45,33±15,46 and 42,82±12,31, respectively) without any gastroenterological pathology in the anamnesis , patients with chronic non-atrophic gastritis (188 people) and chronic atrophic gastritis (137 people). A close relationship was established between the presence of the CagA gene, activity and the degree of contamination for chronic non-atrophic gastritis: for a low degree of contamination, Fisher’s exact test was = 0.002, p<0.05, for a moderate degree - 0.012, p<0.05, for a high degree - 0,012, p<0.05. Accordingly, in chronic atrophic gastritis: for a low degree of contamination Fisher’s exact test = 0.011, p<0.05, for a moderate degree - 0.003, p<0.05, for a high degree - 0.001, p<0.05. There is also a close relationship between the degree of contamination and the activity of chronic gastritis: in patients with a high degree of contamination, CG activity was determined, as a rule, for stage 2-3. In our study, the inflammatory response depended on the presence or absence of the H. pylori strain in the patient, which contains the CagA genotype, which, in our opinion, plays a key role in triggering a cascade of inflammatory changes in the GM and progression of chronic gastritis.