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【medical-news】科学家鉴定出败血症性休克易感基
Scientists identify a septic shock susceptibility gene
In the November 15th issue of G&D, Dr. Robert Schneider and colleagues at NYU School of Medicine report that the AUF1 gene underlies susceptibility to septic shock.
Septic shock often follows a bacterial infection, and is characterized by the overwhelming release of pro-inflammatory cytokines by the body's immune system. This uncontrolled, systemic inflammatory response leads to dangerously low blood pressure and, ultimately, organ failure. One quarter to one half of sepsis patients die, making it the leading cause of hospital deaths in the US.
Dr. Schneider and colleagues demonstrate that the protein encoded by the AUF1 gene destabilizes the mRNA precursors of important pro-inflammatory cytokines. To better understand the role of AUF1 in septic shock, the scientists engineered a strain of transgenic mice deficient in the AUF1 gene, and then exposed them to bacterial endotoxin.
Dr. Schneider and colleagues observed that AUF1-deficinet mice were more sensitive to endotoxin-induced septic shock, displaying an exacerbated pro-inflammatory response and higher mortality rates. They found that AUF1 normally attenuates the immune response by limiting expression of two specific cytokines ?TNFalpha and IL-1beta. In fact, treatment of AUF1-deficient mice with antibodies to neutralize TNFalpha and IL-1beta effectively combated endotoxic shock.
Further research is needed to delineate precisely how AUF1 regulates TNFalpha and IL-1beta, but Dr. Schneider is confident that "AUF1 is a key factor involved in septic shock, and its identification provides an important new target for development of agents to reduce mortality from this life-threatening condition."
### 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 Scientists identify a septic shock susceptibility gene
科学家鉴定出一个败血症性休克易患基因
In the November 15th issue of G&D, Dr. Robert Schneider and colleagues at NYU School of Medicine report that the AUF1 gene underlies susceptibility to septic shock.
在11月15日发表的普通诊断学杂志上，NYU医学院obert Schneide博士和同事报道AUF1基因是败血症性休克的易患基因。
Septic shock often follows a bacterial infection, and is characterized by the overwhelming release of pro-inflammatory cytokines by the body's immune system. This uncontrolled, systemic inflammatory response leads to dangerously low blood pressure and, ultimately, organ failure. One quarter to one half of sepsis patients die, making it the leading cause of hospital deaths in the US.
败血症性休克常发生在细菌感染后，以机体免疫系统释放出大量的致炎(炎症前)细胞因子为特征。这种不受控制的系统性炎症反应会导致危险的低血压，最终器官衰竭。由于四分之一到一半左右的败血病病人死亡，因此此病成为美国医院死亡的主导原因。
Dr. Schneider and colleagues demonstrate that the protein encoded by the AUF1 gene destabilizes the mRNA precursors of important pro-inflammatory cytokines. To better understand the role of AUF1 in septic shock, the scientists engineered a strain of transgenic mice deficient in the AUF1 gene, and then exposed them to bacterial endotoxin.
Schneider博士及其同事证明由AUF1基因编码的蛋白可使重要的致炎(炎症前)细胞因子前体mRNA不稳定。为了更好了解AUF1在败血症性休克中的作用，科学家构造了一种缺少AUF1的转基因小鼠模型，并把这些小鼠感染细菌性内毒素。
Dr. Schneider and colleagues observed that AUF1-deficinet mice were more sensitive to endotoxin-induced septic shock, displaying an exacerbated pro-inflammatory response and higher mortality rates. They found that AUF1 normally attenuates the immune response by limiting expression of two specific cytokines ?TNFalpha and IL-1beta. In fact, treatment of AUF1-deficient mice with antibodies to neutralize TNFalpha and IL-1beta effectively combated endotoxic shock.
Schneider博士及其同事发现AUF1缺陷小鼠对内毒素引发的败血症性休克更敏感，显现出更严重的促炎症反应和更高的死亡率。他们发现AUF1通常通过限制两种特殊因子TNFalpha 和 IL-1beta来减缓免疫反应。事实上，用能中和TNFalpha 和 IL-1beta两种因子的抗体来治疗AUF1缺陷小鼠可有效治疗内毒素性休克。
Further research is needed to delineate precisely how AUF1 regulates TNFalpha and IL-1beta, but Dr. Schneider is confident that "AUF1 is a key factor involved in septic shock, and its identification provides an important new target for development of agents to reduce mortality from this life-threatening condition."
关于AUF1如何调节TNFalpha and IL-1beta还需要进一步研究才能准确阐明。但是Schneider博士深信AUF1基因是败血症性休克疾病的关键因子，它的鉴定为研究新型药物减轻此病死亡率提供了新的靶标。
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作者:admin@医学,生命科学 2010-11-06 05:11
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