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Evaluation of IL-17F A7488G polymorphism in Helicobacter pylori-infected patients: a case–control study

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Objective: Interleukin 17 (IL-17) plays an important role in the inflammation of the gastric mucosa and, in severe cases, the development of gastric cancer. Thus, the authors aimed to evaluate the IL-17F A7488G polymorphism in Helicobacter pylori (H. pylori) patients. Patients and methods: A total of 86 adults (in two H. pylori-positive and H. pylori-negative groups) were included in the study. To identify the infection, rapid urease test and polymerase chain reaction (PCR) were performed. The cagA gene was also evaluated as a bacterial virulence factor. PCR–restriction fragment length polymorphism was used to investigate the IL-17F A7488G polymorphism in gastric biopsies using the NlaIII enzyme. Results: 96.5% of patients in both groups did not show any mutation and had AA genotype, and only three patients infected with cagA-carrying H. pylori strains had polymorphism in the IL-17F A7488G gene, which included AG (one case) and GG (two cases) patterns. No significant relationship was found between these polymorphisms in the two groups of H. pylori-positive and H. pylori-negative patients, while, interestingly, a significant difference was observed between the polymorphisms and the presence of the cagA gene. Conclusion: This report is one of the first to demonstrate the association of IL-17F A7488G polymorphism with H. pylori infection and the presence of the cagA gene. Although no significant association between IL-17F polymorphism and H. pylori infection was found in the population of this study, the patients with mutated genotypes were positive for the cagA gene, which was statistically significant. Therefore, the possibility of the role of pathogenic strains in causing mutations in cytokine genes is more conceivable.
Title: Evaluation of IL-17F A7488G polymorphism in Helicobacter pylori-infected patients: a case–control study
Description:
Objective: Interleukin 17 (IL-17) plays an important role in the inflammation of the gastric mucosa and, in severe cases, the development of gastric cancer.
Thus, the authors aimed to evaluate the IL-17F A7488G polymorphism in Helicobacter pylori (H.
pylori) patients.
Patients and methods: A total of 86 adults (in two H.
pylori-positive and H.
pylori-negative groups) were included in the study.
To identify the infection, rapid urease test and polymerase chain reaction (PCR) were performed.
The cagA gene was also evaluated as a bacterial virulence factor.
PCR–restriction fragment length polymorphism was used to investigate the IL-17F A7488G polymorphism in gastric biopsies using the NlaIII enzyme.
Results: 96.
5% of patients in both groups did not show any mutation and had AA genotype, and only three patients infected with cagA-carrying H.
pylori strains had polymorphism in the IL-17F A7488G gene, which included AG (one case) and GG (two cases) patterns.
No significant relationship was found between these polymorphisms in the two groups of H.
pylori-positive and H.
pylori-negative patients, while, interestingly, a significant difference was observed between the polymorphisms and the presence of the cagA gene.
Conclusion: This report is one of the first to demonstrate the association of IL-17F A7488G polymorphism with H.
pylori infection and the presence of the cagA gene.
Although no significant association between IL-17F polymorphism and H.
pylori infection was found in the population of this study, the patients with mutated genotypes were positive for the cagA gene, which was statistically significant.
Therefore, the possibility of the role of pathogenic strains in causing mutations in cytokine genes is more conceivable.

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