INTERLEUKIN-1 RECEPTOR ANTAGONIST REDUCES MORTALITY FROM ENDOTOXIN-SHOCK
INTERLEUKIN-1 RECEPTOR ANTAGONIST REDUCES MORTALITY FROM ENDOTOXIN-SHOCK
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DOI：
10.1038/348550a0
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发表时间：
1990-12-06
期刊：
影响因子：
64.8
通讯作者：
THOMPSON, RC
中科院分区：
文献类型：
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作者：
OHLSSON, K;BJORK, P;THOMPSON, RC
入院的 1,000 名患者中约有 5 名出现细菌性败血症，导致休克 1，尽管接受抗生素治疗，其死亡率仍然很高 2。感染导致低血压和组织灌注不良，并最终导致多个器官系统衰竭。细菌内毒素被认为是革兰氏阴性败血症休克的直接原因，因为它可以引起动物休克3，而抗内毒素的抗体可以预防动物4和人类5-7的革兰氏阴性休克。但是，感染性休克的症状是内毒素诱导宿主细胞因子作用的结果。细胞因子白介素-1被认为是感染性休克的重要介质，因为它可以诱发心动过速和低血压，并与肿瘤坏死因子协同作用，导致组织损伤8和死亡9。我们现在报道，一种特定的白细胞介素 1 受体拮抗剂可降低兔子内毒素引起的休克的致死率，表明白细胞介素 1 确实在内毒素休克中发挥重要作用。
ABOUT five out of 1,000 patients admitted to hospital develop bacterial sepsis leading to shock1, the mortality rate for which is high despite antibiotic therapy2. The infection results in hypotension and poor tissue perfusion, and eventually leads to the failure of several organ systems. Bacterial endotoxin is thought to be the direct cause of shock in Gram-negative sepsis, because it can cause shock in animals3, and antibodies against endotoxin prevent Gram-negative shock in animals4and in humans5–7. But, the symptoms of septic shock are the result of the actions of host cytokines induced by the endotoxin. The cytokiue interleukin-1 has been implicated as an important mediator of septic shock because it can induce tachycardia and hypotension and act synergistically with tumour necrosis factor to cause tissue damage8and death9. We now report that a specific interleukin-1 receptor antagonist reduces the lethality of endotoxin-induced shock in rabbits, indicating that interleukin-1 does indeed play an important part in endotoxin shock.