BACKGROUND AND OBJECTIVE:A variety of cytokines are involved in the incidence and development of bronchial asthma. This study was designed to reveal the relationship among genetic polymorphism of cytokine genes, expression levels of cytokines and incidence of bronchial asthma. METHODS:We analyzed 14 single nucleotide polymorphism loci in the 10 major cytokine genes plus plasma protein levels of 7 proteins in the bronchial asthma patients (n = 108) and the healthy population (n = 88) of the Han people in northern China. The polymorphism-based genotypes were identified by the sequence-specific primer-polymerase chain reaction. The plasma protein levels were determined by enzyme-linked immunoassay. Bioinformatics analysis was applied to further data processing. RESULTS:Data presented here showed that the 6 polymorphism loci were significantly correlated with the incidence of asthma (p < 0.05). Two of them, IL-2 (-330) and IL-2 (+166), constituted a linkage disequilibrium block. The GG haplotype of this block gave a relatively higher correlation with asthma (p = 0.0767). The plasma protein levels of IgE, IL-6 and IL-1 beta correlated with a number of polymorphism loci tested (p < 0.05), of which IgE gave the most significant correlation. The plasma IL-10 and IL-12 levels of the patients in the asthma group were significantly lower than those of the healthy adults in the control group (p < 0.05), while IgE gave the opposite result (p < 0.0001). We constructed a prototype of the metabolic and regulatory network composed of bronchial asthma-related proteins. In this network, IL-6 and TNF-alpha, were found with a high degree (D = 343 and 235, respectively) and IL-1beta with a moderate degree of connection (D = 155). CONCLUSIONS:We have found that various degrees of correlation with cytokine genes and protein expression of single nucleotide polymorphism in bronchial asthma. IL-6 and IL-1beta appear to play important biological roles in the pathogenesis of asthma. During the analysis of correlation between genetic polymorphism and a complex disease, the effects of environmental factors should be taken into account. The information at the protein level should be fully developed and the bioinformatics techniques can be used for the comprehensive analysis, to have a deep understanding of molecular mechanisms of incidence and development of diseases.

译文

背景与目的:多种细胞因子参与支气管哮喘的发生和发展。本研究旨在揭示细胞因子基因遗传多态性,细胞因子表达水平和支气管哮喘发生率之间的关系。
方法:我们分析了中国北方汉族支气管哮喘患者(n = 108)和健康人群(n = 88)中10个主要细胞因子基因的14个单核苷酸多态性位点以及7种蛋白的血浆蛋白水平。通过序列特异性引物-聚合酶链反应鉴定了基于多态性的基因型。通过酶联免疫测定法测定血浆蛋白水平。生物信息学分析被应用于进一步的数据处理。
结果:这里显示的数据表明6个多态性位点与哮喘的发生率显着相关(p <0.05)。 IL-2(-330)和IL-2(166)中的两个构成了连锁不平衡嵌段。该区域的GG单倍型与哮喘的相关性相对较高(p = 0.0767)。 IgE,IL-6和IL-1β的血浆蛋白水平与测试的多个多态性基因座相关(p <0.05),其中IgE的相关性最为显着。哮喘组患者的血浆IL-10和IL-12水平显着低于对照组健康成年人(p <0.05),而IgE则相反(p <0.0001)。我们构建了由支气管哮喘相关蛋白组成的代谢和调节网络的原型。在该网络中,发现IL-6和TNF-α的程度较高(分别为D = 343和235),而IL-1beta的连接程度为中等(D = 155)。
结论:我们发现支气管哮喘与细胞因子基因和单核苷酸多态性的蛋白质表达有不同程度的相关性。 IL-6和IL-1beta在哮喘的发病机理中似乎起着重要的生物学作用。在分析遗传多态性与复杂疾病之间的相关性时,应考虑环境因素的影响。应该充分开发蛋白质水平的信息,并可以使用生物信息学技术进行综合分析,以深刻理解疾病的发病和发展的分子机制。

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