Interleukin 10 reduces the release of tumor necrosis factor and prevents lethality in experimental endotoxemia.
Interleukin 10 reduces the release of tumor necrosis factor and prevents lethality in experimental endotoxemia.
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DOI：
10.1084/jem.177.2.547
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发表时间：
1993-02-01
期刊：
影响因子：
--
通讯作者：
Velu T
中科院分区：
文献类型：
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作者：
Gérard C;Bruyns C;Marchant A;Abramowicz D;Vandenabeele P;Delvaux A;Fiers W;Goldman M;Velu T
由于其能够有效地抑制激活的巨噬细胞在体外产生细胞因子，我们假设，白细胞介素（IL）10可能是特别感兴趣的，在防止内毒素诱导的毒性。因此，我们研究了在小鼠中脂多糖（LPS）攻击之前施用IL-10的效果。低至10 U的IL-10预处理后，循环中LPS诱导的肿瘤坏死因子（TNF）释放量显著减少。IL-10还有效地防止了注射100微克LPS产生的体温过低。最后，单次注射1,000 U IL-10的预处理完全防止了500微克LPS攻击后的死亡，500微克LPS的剂量在50%的对照小鼠中是致死的。我们的结论是，IL-10抑制体内TNF的分泌，并保护对内毒素的致死性感染性休克小鼠模型。
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.