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Theα1ATandTIMP-1Gene Polymorphism in the Development of Asthma

机译：哮喘发展中的α1AT和TIMP-1基因多态性

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Asthma has been an inflammatory disorder accompanied by tissue remodeling and protease-antiprotease imbalance in lungs. The SNPs ofalpha-1 antitrypsin(α1AT) andtissue inhibitor of metalloproteinase-1(TIMP-1) genes were studied for their association with asthma. Genotyping ofα1ATandTIMP-1genes was performed in 202 asthmatics and 204 controls. Serum levels ofα1AT, TIMP-1 and cytokines were estimated to find if the interplay between genotypes and cellular biomarkers determines the pathogenesis of asthma. The analysis of results showed significantly low level ofα1AT in the serum of asthmatics as compared to controls (P=0.001), whereas cytokines were elevated in patients. No significant difference was observed in the concentration of TIMP-1 in patients and controls. Genotyping led to the identification of 3 SNPs (Val213Ala, Glu363Lys, and Glu376Asp) inα1ATgene. The novel SNP Glu363Lys ofα1ATwas found to be associated with asthma (P=0.001). The analysis ofTIMP-1gene showed the occurrence of seven SNPs, including a novel intronic SNP at base G3774A. The allele frequency of G3774A and Phe124Phe was significantly higher in asthmatics as compared to controls. Thus, the SNP Glu363Lys ofα1ATand G3774A and Phe124Phe ofTIMP-1could be important genetic markers for use in better management of the disease.
机译：哮喘是一种炎症性疾病，伴有肺部组织重塑和蛋白酶-抗蛋白酶失衡。研究了α-1抗胰蛋白酶（α1AT）和金属蛋白酶-1（TIMP-1）组织抑制剂的SNP与哮喘的关系。在202名哮喘患者和204名对照组中进行了α1AT和TIMP-1基因的基因分型。估计血清中α1AT，TIMP-1和细胞因子的水平，以确定基因型和细胞生物标志物之间的相互作用是否决定哮喘的发病机理。结果分析表明，与对照组相比，哮喘患者血清中的α1AT水平明显较低（P = 0.001），而患者的细胞因子却升高了。在患者和对照组中，TIMP-1的浓度未见明显差异。基因分型导致在α1AT基因中鉴定出3个SNP（Val213Ala，Glu363Lys和Glu376Asp）。发现新的α1ATSNP Glu363Lys与哮喘有关（P = 0.001）。 TIMP-1基因的分析表明，出现了七个SNP，包括在碱基G3774A处一个新的内含子SNP。与对照组相比，哮喘患者中G3774A和Phe124Phe的等位基因频率明显更高。因此，α1AT的SNP Glu363Lys和TIMP-1的G3774A和Phe124Phe可能是重要的遗传标记，可用于更好地控制该疾病。

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