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[脓毒症休克中的白细胞介素与肿瘤坏死因子]

[Interleukins and TNF in septic shock].

作者信息

Guidet B, Staikowsky F, Offenstadt G

机构信息

Service de réanimation polyvalente, hôpital Saint-Antoine, Paris.

出版信息

Rev Prat. 1993 Jan 1;43(1):13-7.

PMID:8469892
Abstract

Tumor necrosis factor alpha (TNF alpha) and interleukins (IL) are the principal cytokines involved in the clinical and biological manifestations of septic shock. Their secretion are triggered mainly by endotoxin, but products of Gram positive cocci as well as of virus or of parasites are equally effective. Cytokines represent a normal protective defense against infection, but an excessive production have toxic effects. In experimental models of endotoxinemia, TNF alpha is the first cytokine produced, then IL-1 and IL-6. Other inflammatory mediators are secreted later. Thus it seems logical to try to modulate cytokine production or actions. However, several questions remains since experimental data are sometimes not applicable too human diseases, cytokines are organised in a network with several interaction. It is too early to propose routine anti-cytokines drugs in septic shock.

摘要

肿瘤坏死因子α(TNFα)和白细胞介素(IL)是参与脓毒性休克临床和生物学表现的主要细胞因子。它们的分泌主要由内毒素触发,但革兰氏阳性球菌以及病毒或寄生虫的产物也同样有效。细胞因子代表了针对感染的正常保护性防御,但过量产生则具有毒性作用。在内毒素血症的实验模型中,TNFα是首先产生的细胞因子,然后是IL-1和IL-6。其他炎症介质随后分泌。因此,尝试调节细胞因子的产生或作用似乎是合乎逻辑的。然而,由于实验数据有时不适用于人类疾病,细胞因子以具有多种相互作用的网络形式组织,仍存在几个问题。在脓毒性休克中提出常规抗细胞因子药物还为时过早。

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