Ivy Bastos Ramis1, Júlia Silveira Vianna2, Carla Vitola Gonçalves3, Andrea von Groll3, Odir Antônio Dellagostin2, Pedro Eduardo Almeida da Silva4. 1. Centro de Desenvolvimento Tecnológico-Universidade Federal de Pelotas (UFPel), Pelotas, Rio Grande do Sul, Brazil. Electronic address: ivynha_@hotmail.com. 2. Centro de Desenvolvimento Tecnológico-Universidade Federal de Pelotas (UFPel), Pelotas, Rio Grande do Sul, Brazil. 3. Núcleo de Pesquisa em Microbiologia Médica-Universidade Federal do Rio Grande (FURG), Rio Grande, Rio Grande do Sul, Brazil. 4. Centro de Desenvolvimento Tecnológico-Universidade Federal de Pelotas (UFPel), Pelotas, Rio Grande do Sul, Brazil; Núcleo de Pesquisa em Microbiologia Médica-Universidade Federal do Rio Grande (FURG), Rio Grande, Rio Grande do Sul, Brazil.
Abstract
BACKGROUND/ PURPOSE: Helicobacter pylori-induced gastric mucosal inflammation is mediated by proinflammatory and anti-inflammatory cytokines. Polymorphisms in genes that code cytokines influence cytokine secretion levels and appear to contribute to the risk of gastric diseases. In this sense, we performed this study to identify the polymorphisms in the IL-6, IL-8, and IL-10 genes and their associations with H. pylori infection and gastric pathologies. METHODS: Gastric biopsy samples of 151 patients infected with H. pylori and 76 uninfected individuals were used. Helicobacter pylori infection was diagnosed by histological examination and the detection of the ureA and glmM genes. The polymorphisms in the IL-6 (at position -174), IL-8 (at position -251), and IL-10 (at position -819) were detected by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: Among the genetic polymorphisms studied, we observed that only the presence of the A allele at position -251 of the IL-8 gene was significantly associated with H. pylori infection. In addition, patient carriers of the A/A genotype at position -251 of the IL-8 gene and carriers of the T allele at position -819 of the IL-10 gene had an increased risk of peptic ulcer disease in the presence of H. pylori infection. We did not find a correlation between polymorphisms in the IL-6, IL-8, and IL-10 genes and a higher risk of gastric carcinoma. CONCLUSION: We demonstrated that polymorphisms in the IL-8 gene was significantly associated with H. pylori infection. Furthermore, polymorphisms in the IL-8 and IL-10 genes were associated with an enhanced risk of peptic ulcer disease in H. pylori-positive patients.
BACKGROUND/ PURPOSE:Helicobacter pylori-induced gastric mucosal inflammation is mediated by proinflammatory and anti-inflammatory cytokines. Polymorphisms in genes that code cytokines influence cytokine secretion levels and appear to contribute to the risk of gastric diseases. In this sense, we performed this study to identify the polymorphisms in the IL-6, IL-8, and IL-10 genes and their associations with H. pyloriinfection and gastric pathologies. METHODS: Gastric biopsy samples of 151 patients infected with H. pylori and 76 uninfected individuals were used. Helicobacter pyloriinfection was diagnosed by histological examination and the detection of the ureA and glmM genes. The polymorphisms in the IL-6 (at position -174), IL-8 (at position -251), and IL-10 (at position -819) were detected by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: Among the genetic polymorphisms studied, we observed that only the presence of the A allele at position -251 of the IL-8 gene was significantly associated with H. pyloriinfection. In addition, patient carriers of the A/A genotype at position -251 of the IL-8 gene and carriers of the T allele at position -819 of the IL-10 gene had an increased risk of peptic ulcer disease in the presence of H. pyloriinfection. We did not find a correlation between polymorphisms in the IL-6, IL-8, and IL-10 genes and a higher risk of gastric carcinoma. CONCLUSION: We demonstrated that polymorphisms in the IL-8 gene was significantly associated with H. pyloriinfection. Furthermore, polymorphisms in the IL-8 and IL-10 genes were associated with an enhanced risk of peptic ulcer disease in H. pylori-positive patients.