Investigation of the clinical correlation of IL-6, IL-8, IL-10, IL-17A, AND IL-19 gene expressions and mutations in patients with upper gastrointestinal pathology of helicobacter pylori

Helicobacter pylori (H. pylori) is a gastric pathogen that infects more than half of the world's population and the major cause of neoplastic and inflammatory gastroduodenal diseases of the stomach. Today, the association of H. pylori with upper gastrointestinal system (GIS) diseases such as chronic gastritis, peptic ulcer disease, gastric cancer, mucosa-associated lymphoid tissue lymphoma (MALT) has been shown. The pathophysiological key to H. pylori infection is the result of the inflammatory response of the gastric mucosa by inflammatory cytokines produced by epithelial cells against H. pylori antigens. This gastric mucosal inflammation induced by H. pylori is mediated by proinflammatory and anti-inflammatory cytokines. Polymorphisms in genes encoding cytokines are thought to affect cytokine secretion levels and are determinative for the prognosis of gastroduodenal pathology. Gastric pathologies are develop in a complex interaction between the genetic structure of the host and the H. pylori virulence genes. It is thought that polymorphisms in genes encoding cytokines such as IL-6, IL-8, IL-10, IL-17A and IL-19 in patients affect the secretion levels of cytokines and cause the development of GIS pathology. For this reason, our study we aimed to determine the polymorphisms of these genes in patients and their relationship with H. pylori infection and gastric pathologies. Materials and Methods: For this purpose, samples of 200 patients who applied to inpatient treatment institutions in our region with upper GIS complaints and whose gastric biopsy samples were taken with endoscopy for diagnostic purposes, and H. pylori strains isolated from these samples were included in the study. As a control group, we used whole blood samples from 50 volunteer participants who did not have any upper GIS complaints. Patient biopsy specimens were evaluated by molecular methods both in terms of the presence of the H. pylori ureC gene and IL-6-174, IL-8-251, IL-10-819, IL-17A, and IL-19 accompanying various GIS pathologies due to H. pylori. The polymorphism of the genes was genotyped by PCR-RFLP. Also, the polymorphisms of the gene regions specified in the control group were genotyped by PCR RFLP. Results: As a result of glmM-PCR analysis, H. pylori DNA was detected in 69 (34,5%) of 200 symptomatic patients. In the IL-8 -251 polymorphism, the T/A genotype was 73,91% in the patient group, 48% in the control group, and in the IL-17A polymorphism, the G/A genotype was 56,52% in patient group, while it was 42% in the control group. No correlation was found between IL-6-174 and IL-10-819 polymorphism and gastroduodenal pathology. Conclution: In H. pylori infection, cytokine gene polymorphisms affect gastric inflammation. This interaction, which is considered as the possible main pathway between polymorphisms in these genes and H. pylori infection, causes different gastric diseases. Determination of host genotypes can be used as a target in the treatment of H. pylori infection in high-risk GIS patients. Keywords: Helicobacter pylori, gastric pathology, cytokine, interleukin