Interleukin-10 gene-627 allele variants, not interleukin-1 beta gene and receptor antagonist gene polymorphisms, are associated with atopic bronchial asthma

Interleukin-10 gene-627 allele variants, not interleukin-1 beta gene and receptor antagonist gene polymorphisms, are associated with atopic bronchial asthma
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DOI:
10.1002/jcla.10088
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发表时间:
2003-01-01
影响因子:
2.7
通讯作者:
Tsai, FJ
Tsai, FJ
中科院分区:
医学4区
文献类型:
--
作者:
Hang, LW;Hsia, TC;Tsai, FJ

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哮喘是一种气道高反应性疾病,其特征是表达多种炎症基因,包括细胞因子。白细胞介素-I 和白细胞介素-10(IL-1 和 IL-10)是可能在炎症过程中发挥作用的细胞因子,因此被认为参与支气管哮喘的发病机制。本研究的目的是检测IL-1基因启动子区和外显子5、IL-1Ra基因内含子2和IL-10基因-627核苷酸(C/A)的多态性是否可以作为支气管哮喘易感性的遗传标记。本研究对由 47 名健康志愿者和 117 名支气管哮喘患者组成的正常对照组进行了检查。我们通过聚合酶链式反应 (PCR) 分析了 IL-1Ra 基因内含子 2 处可变数量的串联重复的多态性。分别通过核酸内切酶Ava I和Taq I对启动子区和外显子5的IL-1基因多态性进行基于PCR的限制性分析。通过基于 PCR 的限制性分析研究了 IL-10 基因 -627 C/A 多态性。哮喘患者IL-10基因CC纯合子分布显着低于对照组(P=0.013, OR=3.599, 95% CI=1.240与10.441相似)。与对照组相比,IL-1基因的多态性研究并未显示与支气管哮喘有任何显着相关性(启动子区域通过卡方检验,P=0.627;外显子5区域通过Fisher精确检验,P=0.403)。在对照组中,通过 PCR 仅鉴定出对应于 86 碱基对序列重复的一个和两个拷贝的 IL-1Ra 基因的两个等位基因。在哮喘患者组中发现了三个等位基因。结果显示正常人和哮喘患者之间没有显着差异(P=0.454,​​Fisher精确检验)。 IL-10 基因-627“A”等位基因是发生特应性哮喘的相关危险因素。
Asthma is an airway hyperresponsive disease characterized by the expression of multiple inflammatory genes, including cytokines. Interleukin-I and interleukin-10 (IL-1 and IL-10) are cytokines that might play a role in the process of inflammation and are therefore considered to be involved in the pathogenesis of bronchial asthma. The aim of this study was to test whether the polymorphisms of the promoter region and exon 5 of the IL-1 gene, intron 2 of the IL-1 Ra gene, and -627 nucleotiDe (C/A) of the IL-10 gene could be genetic markers for the susceptibility of bronchial asthma. A normal control group made up of 47 healthy volunteers and 117 patients with bronchial asthma were examined in this study. We analyzed the variable number of tandem repeats at intron 2 of the IL-1Ra gene for the polymorphisms by polymerase chain reaction (PCR). PCR-based restriction analysis of the IL-1 gene polymorphisms of the promoter region and exon 5 was carried out by the endonucleases Ava I and Taq I, respectively. The IL-10 gene -627 C/A polymorphisms were investigated by PCR-based restriction analysis. The distribution of CC homozygotes in the IL-10 gene was significantly lower in asthma patients than in controls (P=0.013, OR=3.599, 95% CI=1.240similar to10.441). The polymorphisms studied in the IL-1 genes did not reveal any significant association with bronchial asthma when compared with the control group (promoter region by chi-square test, P=0.627; exon 5 region by Fisher's exact test, P=0.403). Only two alleles of the IL-1Ra gene corresponding to one and two copies of an 86-base pair sequence repeat were identified by PCR in the control group. There were three alleles found in the asthmatic patient group. The results revealed no significant differences between normal individuals and asthma patients (P=0.454, Fisher's exact test). The IL-10 gene -627 "A" allele is an associated risk factor of developing atopic asthma.