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白细胞介素10可减少肿瘤坏死因子的释放,并预防实验性内毒素血症中的致死情况。

Interleukin 10 reduces the release of tumor necrosis factor and prevents lethality in experimental endotoxemia.

作者信息

Gérard C, Bruyns C, Marchant A, Abramowicz D, Vandenabeele P, Delvaux A, Fiers W, Goldman M, Velu T

机构信息

Institut de Recherche Interdisciplinaire, Université Libre de Bruxelles, Belgium.

出版信息

J Exp Med. 1993 Feb 1;177(2):547-50. doi: 10.1084/jem.177.2.547.

DOI:10.1084/jem.177.2.547
PMID:8426124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2190913/
Abstract

Because of its ability to efficiently inhibit in vitro cytokine production by activated macrophages, we hypothesized that interleukin (IL) 10 might be of particular interest in preventing endotoxin-induced toxicity. We therefore examined the effects of IL-10 administration before lipopolysaccharide (LPS) challenge in mice. A marked reduction in the amounts of LPS-induced tumor necrosis factor (TNF) release in the circulation was observed after IL-10 pretreatment at doses at low as 10 U. IL-10 also efficiently prevented the hypothermia generated by the injection of 100 micrograms LPS. Finally, pretreatment with a single injection of 1,000 U IL-10 completely prevented the mortality consecutive to the challenge with 500 micrograms LPS, a dose that was lethal in 50% of the control mice. We conclude that IL-10 inhibits in vivo TNF secretion and protects against the lethality of endotoxin in a murine model of septic shock.

摘要

由于白细胞介素(IL)-10能够有效抑制体外活化巨噬细胞产生细胞因子,我们推测IL-10在预防内毒素诱导的毒性方面可能具有特殊意义。因此,我们研究了在小鼠脂多糖(LPS)攻击前给予IL-10的效果。在低至10 U剂量的IL-10预处理后,观察到循环中LPS诱导的肿瘤坏死因子(TNF)释放量显著减少。IL-10还能有效预防注射100微克LPS所产生的体温过低。最后,单次注射1000 U IL-10预处理完全预防了500微克LPS攻击后的死亡,该剂量在50%的对照小鼠中是致命的。我们得出结论,在脓毒症休克小鼠模型中,IL-10可抑制体内TNF分泌并保护机体免受内毒素致死作用。

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Interleukin 10 reduces the release of tumor necrosis factor and prevents lethality in experimental endotoxemia.白细胞介素10可减少肿瘤坏死因子的释放,并预防实验性内毒素血症中的致死情况。
J Exp Med. 1993 Feb 1;177(2):547-50. doi: 10.1084/jem.177.2.547.
2
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本文引用的文献

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