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首页> 外文期刊>International journal of immunogenetics >Characterization of tumour necrosis factor-alpha genetic variants and mRNA expression in patients with severe sepsis.
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Characterization of tumour necrosis factor-alpha genetic variants and mRNA expression in patients with severe sepsis.

机译：严重败血症患者的肿瘤坏死因子-α基因变异和mRNA表达的表征。

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Tumour necrosis factor-alpha (TNFalpha) has been implicated in the pathogenicity of severe sepsis by both genetic association studies and animal models. Conflicting functional data have emerged in relation to genetic variants and TNFalpha protein production. Therefore, we assessed the functionality of TNFalpha genetic variants in terms of mRNA production and their potential influence on outcome in the setting of severe sepsis. Sixty-two Irish Caucasian patients presenting with severe sepsis were recruited and TNFalpha mRNA and protein levels were quantified. Patient DNA was analysed for the presence of common promoter polymorphisms and haplotypes were inferred. An A allele at position -863 was associated with more TNFalpha mRNA on day 1 compared to C homozygotes (P = 0.037). There was a trend for G homozygotes at position -308 to produce more TNFalpha mRNA on day 1 than those carrying an A allele (P = 0.059). The presence of an A allele at -863 was associated with greater levels of TNFalpha mRNA in comparison with patients carrying the A allele at -308 on day 1 (P = 0.02). Patients homozygous for the A allele at position -308 had a higher mortality than those carrying the G allele (P = 0.01). Our data are consistent with recent reports suggesting that a deficient proinflammatory response may be harmful in human sepsis. This deficient inflammatory response may be mediated in part by polymorphisms in the TNFalpha promoter.
机译：遗传关联研究和动物模型均表明，肿瘤坏死因子-α（TNFalpha）与严重败血症的致病性有关。与遗传变异和TNFα蛋白产生有关的功能数据相互矛盾。因此，我们根据mRNA的产生及其在严重败血症中对预后的潜在影响评估了TNFalpha遗传变异的功能。招募了62名患有严重败血症的爱尔兰高加索患者，并对TNFalpha mRNA和蛋白质水平进行了定量。分析患者DNA中常见启动子多态性的存在，并推断单倍型。与C纯合子相比，第-863天的A等位基因与更多的TNFalpha mRNA相关（P = 0.037）。在第-308位的G纯合子有一种趋势，在第1天比携带A等位基因的纯合子产生更多的TNFalpha mRNA（P = 0.059）。与在第1天在-308携带A等位基因的患者相比，在-863处存在A等位基因与更高水平的TNFalpha mRNA相关（P = 0.02）。在-308位纯合的A等位基因患者的死亡率高于携带G等位基因的患者（P = 0.01）。我们的数据与最近的报道一致，提示缺乏促炎反应可能对人类败血症有害。这种不足的炎症反应可能部分由TNFalpha启动子中的多态性介导。

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