van der Poll T, Marchant A, Buurman W A, Berman L, Keogh C V, Lazarus D D, Nguyen L, Goldman M, Moldawer L L, Lowry S F
Cornell University Medical College, Department of Surgery, New York, NY 10021, USA.
J Immunol. 1995 Dec 1;155(11):5397-401.
IL-10 production during endotoxic shock is part of a protective mechanism that involves IL-10-induced inhibition of TNF synthesis. We sought to determine the role of IL-10 in septic peritonitis induced by cecal ligation and puncture (CLP). CLP led to a rapid induction of IL-10 mRNA in various organs of C57BI/6 mice. In liver, IL-10 mRNA was detectable within 1 h following CLP, while in spleen and lungs, IL-10 mRNA was detected from 2 to 4 h and onward. IL-10 protein became detectable in plasma 2 h after CLP, reaching peak concentrations after 12 h (12.7 +/- 5.7 ng/ml). Pretreatment (-2 h) with anti-IL-10 mAb resulted in higher plasma TNF levels following CLP when compared with mice treated with control mAb. Plasma IL-1 activity and IFN-gamma remained undetectable in virtually all mice. Anti-IL-10 enhanced mortality after CLP (p < 0.05 by log-rank test). Addition of anti-TNF mAb did not influence the increased mortality associated with anti-IL-10 treatment. Septic peritonitis is associated with sustained production of IL-10 in various organs, which serves to protect the host against lethality.
内毒素休克期间白细胞介素-10（IL-10）的产生是一种保护机制的一部分，该机制涉及IL-10诱导的肿瘤坏死因子（TNF）合成抑制。我们试图确定IL-10在盲肠结扎和穿刺（CLP）诱导的脓毒症性腹膜炎中的作用。CLP导致C57BI/6小鼠各器官中IL-10 mRNA迅速诱导产生。在肝脏中，CLP后1小时内可检测到IL-10 mRNA，而在脾脏和肺中，2至4小时及之后可检测到IL-10 mRNA。CLP后2小时血浆中可检测到IL-10蛋白，12小时后达到峰值浓度（12.7±5.7 ng/ml）。与用对照单克隆抗体（mAb）处理的小鼠相比，用抗IL-10 mAb预处理（-2小时）导致CLP后血浆TNF水平更高。几乎所有小鼠的血浆IL-1活性和干扰素-γ（IFN-γ）均未检测到。抗IL-10增加了CLP后的死亡率（对数秩检验，p<0.05）。添加抗TNF mAb并不影响与抗IL-10治疗相关的死亡率增加。脓毒症性腹膜炎与各器官中IL-10的持续产生有关，这有助于保护宿主免于死亡。
