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[目的]探讨白细胞介素-10(IL-10)基因启动子区基因多态性与中国汉族人肺结核发病的关系。[方法]采用病例对照研究设计,选择135例健康对照和141例肺结核患者为研究对象,对肺结核发病影响因素进行问卷调查,应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)分析方法,对全部研究对象的IL-10基因启动子区-1082、-819位点单核苷酸多态性(SNP)进行基因分型,对各危险因素进行单因素分析和多因素非条件Logistic回归分析。[结果]接触史、卡痕、家族史与肺结核的发生有关。IL-10-1082位点各基因型在病例组和对照组中的分布频率未见差别(χ2=0.906,P=0.636)。IL-10-819位点野生型(CC)、突变型杂合子(CT)、突变型纯合子(TT)3种基因型在病例组和对照组中的分布频率不同(χ2=14.376,P=0.001)。在多因素分析中调整接触史、卡痕和家族史后,IL-10-819突变型纯合子(TT)与肺结核发病密切相关,差异有统计学意义,以野生基因型CC为参照,调整后突变型纯合子TT(OR=0.312,95%CI为0.167~0.582),为肺结核发病的保护因素。[结论]IL-10-819位点TT基因型可能与肺结核发病相关。
[Objective] To investigate the relationship between polymorphism of interleukin-10 (IL-10) gene promoter region and pulmonary tuberculosis in Han Chinese. [Methods] A case-control study was designed. 135 healthy controls and 141 pulmonary tuberculosis patients were selected as research subjects. The influencing factors of pulmonary tuberculosis were investigated by questionnaire. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) Methods: Genotypes of -1082 and -819 SNPs in IL-10 gene promoter region of all subjects were genotyped. Univariate analysis and multivariate non-conditional analysis of risk factors Logistic regression analysis. [Results] The contact history, card marks, family history and tuberculosis were related. There was no difference in the frequencies of IL-10-1082 genotypes between case group and control group (χ2 = 0.906, P = 0.636). The genotype frequency of IL-10-819 wild-type (CC), mutant heterozygous (CT) and mutant homozygous (TT) genotypes were different in case and control groups (χ2 = 14.376, P = 0.001). IL-10-819 mutant homozygote (TT) was closely related to the incidence of pulmonary tuberculosis after adjusting for contact history, card marks and family history in multivariate analysis with statistical significance, with reference to the wild type CC, after adjustment Mutant homozygous TT (OR = 0.312,95% CI 0.167 ~ 0.582), for the protection of tuberculosis pathogenesis. [Conclusion] The TT genotype of IL-10-819 may be related to the pathogenesis of pulmonary tuberculosis.