内毒素诱导的新生小鼠致死性可被白细胞介素-10（IL-10）抵消，而抗IL-10会使其加剧。
Endotoxin-induced lethality in neonatal mice is counteracted by interleukin-10 (IL-10) and exacerbated by anti-IL-10.
作者信息
Nicoletti F, Mancuso G, Ciliberti F A, Beninati C, Carbone M, Franco S, Cusumano V
机构信息
Institute of Microbiology, University of Milan, Italy.
出版信息
Clin Diagn Lab Immunol. 1997 Sep;4(5):607-10. doi: 10.1128/cdli.4.5.607-610.1997.
Abstract
The lethal effects occurring in neonatal (<24-h-old) BALB/c mice after challenge with 25 mg of lipopolysaccharide (LPS) per kg of body weight were significantly counteracted by pretreatment with recombinant interleukin-10 (rIL-10; 25 or 50 ng/mouse). Concordantly, blockage of endogenous IL-10 with the SXC1 monoclonal antibody increased LPS-induced mortality. Both IL-10 and SXC1 modulated the release of tumor necrosis factor alpha (TNF-alpha) so that, relative to controls, peak TNF-alpha values after LPS challenge were decreased by rIL-10 and increased by anti-IL-10.
摘要
用每千克体重25毫克脂多糖（LPS）攻击新生（<24小时龄）BALB/c小鼠后出现的致死效应，可通过用重组白细胞介素-10（rIL-10；25或50纳克/小鼠）预处理而得到显著抵消。与此一致的是，用SXC1单克隆抗体阻断内源性IL-10会增加LPS诱导的死亡率。IL-10和SXC1都调节肿瘤坏死因子α（TNF-α）的释放，因此，相对于对照组，LPS攻击后的TNF-α峰值在rIL-10处理后降低，而在抗IL-10处理后升高。
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