ABSTRACT
BACKGROUND: The genes encoding IL9, IL9R, IL17A, and IL17F have recently been implicated in the genetic basis of rhinitis and allergy. AIM: The purpose of this study was to assess the association of the single nucleotide polymorphisms (SNPs) of IL9, IL9R, IL17A, and IL17F and potential interaction of these genes with the determination of IgE levels in women with allergic rhinitis (AR) in Shahrekord, Iran. SUBJECTS AND METHODS: In a case-control study, SNPs from the IL9, IL9R, IL17A, and IL17F were genotyped in 394 random samples including 195 AR patients and 199 normal controls. Enzyme-linked immunosorbent assay was performed for the determination of serum total IgE levels. The Student's t-test was used to compare the differences. The Chi-square test was performed to compare proportions of cases with different clinical features among cases with different genotypes. The genotype and allele frequencies were obtained by direct counting. Hardy-Weinberg equilibrium was tested between cases and controls separately. The relative risk associated with rare alleles was estimated as an odds ratio with 95% confidence interval. P ≤ 0.05 was considered statistically significant. RESULTS: The rs731476 SNP in the IL9R was significantly associated with the AR phenotype in women. No association was found between any of the other SNPs in IL9, IL17A, and IL17F genes and AR. In the gene-gene interaction analysis, we found that IL9R/IL9 genotype rs731476 T-/rs2069885 G conferred a higher risk for AR phenotype development. We also did not find a significant association in terms of IgE levels between cases and controls. CONCLUSION: Our result suggests that the rs731476 SNP located in the IL9R is associated with an increased susceptibility to AR in females. In a subsequent gene-gene interaction analysis, the rs731476 T-/rs2069885 G-genotype combination (IL9R/IL9) has significantly been associated with the development of the AR phenotype.
ABSTRACT
BACKGROUND AND OBJECTIVE: Chronic inflammation is the hallmark of the pathogenesis of H. pylori-induced gastric cancer. IL-17A and IL-17F are inflammatory cytokines expressed by a novel subset of CD4+Th cells and play critical function in inflammation. We evaluated the relationship between IL-17A G197A, IL-17F A7488G and IL23R+2199 A/C polymorphisms with IL-6, IL-17, IL-21, IL-23 and TGF-ß1 mRNAs expression in regard to H. pylori infection with chronic gastritis. MATERIAL AND METHODS: Total RNA and genomic DNA were extracted from gastric biopsies of 58 H. pylori-infected patient with gastritis. Afterward, mucosal IL-6, IL-17, IL-21, IL-23 and TGF-ß1 mRNAs expression and polymorphisms in IL-17A G197A, IL-17F A7488G and IL-23R +2199A/Cin gastric biopsies were determined by real-time PCR and PCR-RFLP. RESULTS: Our results show that IL-17A G197A, IL-17F A7488G andIL23R +2199A/C polymorphisms have no effect on mucosal expression of IL-6, IL-17, IL-21 and TGF-ß1 mRNAs expression in H. pylori-infected patients with chronic gastritis. CONCLUSIONS: These results suggest that IL-17A G197A, IL-17F A7488G and IL23R +2199A/C polymorphisms no alter mucosal cytokine pattern in Iranian patients with H. pylori-associated gastritis diseases.
