The role of cytokine gene polymorphism in the development of unfavorable course of Helicobacter pylori infection

We aimed to evaluate the cytokine gene polymorphism role in predisposing patients with Helicobacter pylori infection to atrophic gastritis and duodenal ulcers. We examined 182 patients with various forms of gastroduodenal pathology. The presence or absence of H. pylori was verified using a combination of histological examination and PCR. Polymerase chain reaction with restriction fragment length polymorphism and allele-specific PCR were used to genotype five key polymorphic loci in the IL-1 (-31, -511), IL-4 (-590), IL-8 (-251), IL-10 (-592), and TNF-α (-308) genes. As a result, we found that the CC (-31) and TT (-511) genotypes of the IL-1 gene are significantly associated with an increased risk of atrophic gastritis (OR = 6.5 and OR = 4.8, respectively), which, in our opinion, is due to hyperproduction of the proinflammatory cytokine and suppression of gastric acid secretion. We found in patents with peptic ulcer disease an increased frequency of the AA IL-10 genotypes (-592) and a decreased frequency of AA IL-8 (-251). The presence IL-4 (-590) allele T is a protective factor (OR = 0.3), and TNF-α (-308) allele A is risk factor for the development of duodenal ulcer disease (OR = 3.7). Thus, cytokine gene polymorphism is a significant factor of genetic predisposition that determines the differentiated risk of developing atrophic gastritis or duodenal ulcer in Helicobacter pylori infection.