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  • 1
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. Helicobacter pylori induces inflammation of gastric mucosa regulated by several interleukins. This study examined associations between anti-Helicobacter pylori immunoglobulin G antibody seropositivity and functional polymorphisms of interleukin-8 T-251 A and interleukin-10 T-819C.Materials and Methods. The subjects were 454 health check-up examinees (126 males and 328 females) without a history of cancer, aged 35–85 years, residing in Nagoya, Japan. After written informed consent was obtained individually, residual blood was anonymously applied for anti-Helicobacter pylori immunoglobulin G antibody testing and genotyping by the polymerase chain reaction with confronting two-pair primers.Results. The genotype frequency of interleukin-8 T-251 A was 52.2% for TT, 39.5% for TA, and 8.3% for AA, and that of interleukin-10 T-819C was 49.5% for TT, 39.9% for TC and 10.6% for CC. Although the differences in the positive rates among the genotypes were not marked, 115 individuals with interleukin-8–251TT (low expression genotype) and interleukin-10–819TT (high expression genotype) had a higher rate (63.5%) than the others (52.0%). Relative to the combination of interleukin-8–251TT and interleukin-10–819TT, the sex-age-adjusted odds ratio for those with the other combinations was 0.62 (95% confidence interval, 0.39–0.98). The adjusted odds ratio among 65 current smokers was 0.13 (0.03–0.61).Conclusions. The observed association suggests that individuals with interleukin-8–251TT and interleukin-10–819TT, a combination presumably causing mild inflammation, have a higher probability of the continuing Helicobacter pylori infection, especially among current smokers.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background.  Gastric atrophy induced by Helicobacter pylori is thought to predispose patients to noncardiac gastric cancer development. However, the host genetic factors that influence the progression of gastric atrophy have not been elucidated. In this study, we examined the effects of cytokine polymorphisms on H. pylori-induced gastric atrophy.Methods.  Blood samples were taken from 454 Japanese subjects. The interleukin-2 (IL-2; T-330G), IL-4 (C-33T), and IL-13 (C-1111T) polymorphisms were genotyped by polymerase chain reaction with confronting two-pair primers (PCR-CTPP). Anti-H. pylori IgG antibody and pepsinogen I and II were measured to diagnose H. pylori infection and atrophic gastritis.Results.  The odds ratios (ORs) for the association between IL-2 polymorphism [OR = 2.78, 95% CI (confidence interval) = 1.26–6.17 (T/T to G/G)] or IL-4 polymorphism [OR = 2.22, 95% CI = 1.01–4.89 (T/C to C/C)] were increased significantly with gastric atrophy, whereas the corresponding OR of IL-13 polymorphism was decreased with gastric atrophy [OR = 0.61, 95% CI = 0.39–0.96 (C/T and T/T to C/C)]. There were no significant H. pylori seropositivity-related differences between these polymorphisms. We examined the relationship between these polymorphisms and gastric atrophy separately in H. pylori-seropositive and -seronegative groups. In the H. pylori-seropositive group, the IL-2 T/T (OR = 2.78, 95% CI = 1.12–6.93) had a significant association with gastric atrophy.Conclusions.  These results reveal that the IL-2 gene polymorphism is associated with an increased risk of gastric atrophy induced by H. pylori infection and might predispose to gastric cancer.
    Type of Medium: Electronic Resource
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