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首页> 外文期刊>Allergy >Combined effect of IL-10 and TGF-beta1 promoter polymorphisms as a risk factor for aspirin-intolerant asthma and rhinosinusitis.
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Combined effect of IL-10 and TGF-beta1 promoter polymorphisms as a risk factor for aspirin-intolerant asthma and rhinosinusitis.

机译：IL-10和TGF-β1启动子多态性的联合作用是阿司匹林耐受性哮喘和鼻窦炎的危险因素。

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BACKGROUND: It has been known that interleukin (IL)-10 promoter polymorphisms at -1082A/G, -819T/C and -592A/C, may influence IL-10 expression and associate with asthma. Interleukin-10 facilitates the regulatory function of transforming growth factor (TGF)-beta. The goal of this study was to investigate a gene-gene interaction between IL-10 and TGF-beta1 polymorphisms in Korean asthmatics with aspirin hypersensitivity. METHODS: Single-nucleotide polymorphism genotyping of IL-10 and TGF-beta1 genes was performed and the functional effect of the IL-10 polymorphisms was analysed applying a luciferase reporter assay and an electrophoretic mobility shift assay. RESULTS: Among the patients with asthma, polymorphism at -1082A/G was significantly associated with the phenotype of aspirin-intolerant asthma, AIA (P = 0.007, P(c) = 0.021). Moreover, a synergistic effect between the TGF-beta1-509C/T and IL-10-1082A/G polymorphisms on the phenotype of AIA was noted; when stratified by the presence of rhinosinusitis, the frequency of rare alleles (the CT or TT genotype of TGF-beta1-509C/T and AG or GG genotype of IL-10-1082A/G) was significantly higher in the patients with AIA (15.2%) when compared with those with ATA (6.3%, P = 0.031; odds ratio 4.111; 95% confidence interval 1.504-11.235). In an in vitro functional assay, the -1082G reporter plasmid exhibited significantly greater promoter activity when compared with the -1082A construct in Jurkat T cells (P = 0.011). Moreover, we found that the transcription factor Myc-associated zinc-finger protein preferentially bound the -1082G allele. CONCLUSION: Our results suggest that IL-10 promoter polymorphisms contribute to the development of AIA and that rhinosinusitis may interact genetically with TGF-beta1.
机译：背景：已知在-1082A / G，-819T / C和-592A / C的白介素（IL）-10启动子多态性可能会影响IL-10的表达并与哮喘相关。白介素10促进转化生长因子（TGF）-β的调节功能。这项研究的目的是调查阿司匹林超敏反应在韩国哮喘患者中IL-10和TGF-β1多态性之间的基因-基因相互作用。方法：对IL-10和TGF-β1基因进行单核苷酸多态性基因分型，并通过荧光素酶报告基因分析和电泳迁移率变动分析分析IL-10多态性的功能作用。结果：在哮喘患者中，-1082A / G的多态性与阿司匹林耐受性哮喘AIA的表型显着相关（P = 0.007，P（c）= 0.021）。此外，注意到TGF-β1-509C/ T和IL-10-1082A / G多态性之间对AIA表型的协同作用。当根据鼻-鼻窦炎的存在进行分层时，AIA患者中罕见等位基因（TGF-beta1-509C / T的CT或TT基因型以及IL-10-1082A / G的AG或GG基因型）的发生频率显着更高（与ATA（6.3％，P = 0.031;优势比4.111; 95％置信区间1.504-11.235）相比，为15.2％）。在体外功能测定中，与Jurkat T细胞中的-1082A构建体相比，-1082G报告质粒表现出明显更高的启动子活性（P = 0.011）。此外，我们发现转录因子Myc相关的锌指蛋白优先结合-1082G等位基因。结论：我们的结果表明IL-10启动子多态性有助于AIA的发展，并且鼻-鼻窦炎可能与TGF-β1发生遗传相互作用。

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