van der Poll T, Jansen P M, Montegut W J, Braxton C C, Calvano S E, Stackpole S A, Smith S R, Swanson S W, Hack C E, Lowry S F, Moldawer L L
Cornell University Medical College, Department of Surgery, New York 10021, USA.
J Immunol. 1997 Feb 15;158(4):1971-5.
IL-10 protects mice from LPS-induced lethality. To determine the effects of IL-10 on LPS-induced inflammatory responses, six Papio anubis baboons were i.v. injected with a sublethal dose of LPS (Salmonella typhimurium; 500 microg/kg) directly preceded by either human rIL-10 (n = 3, 500 microg/kg) or diluent (n = 3). IL-10 strongly inhibited LPS-induced release of TNF, IL-6, IL-8, and IL-12 (all p < 0.05). By contrast, IL-10 did neither influence the activation of the coagulation system (plasma levels of thrombin/antithrombin III complexes), nor the activation of the fibrinolytic system (plasma levels of tissue-type plasminogen activator, plasminogen activator inhibitor type I, and plasmin/alpha 2-antiplasmin complexes). IL-10 modestly attenuated neutrophilic leukocytosis and neutrophil degranulation (plasma concentrations of elastase/alpha1-antitrypsin complexes) (both p < 0.05). Changes in surface TNF receptor expression on circulating granulocytes were not affected by IL-10. These results suggest that during sublethal endotoxemia the predominant anti-inflammatory effect of IL-10 treatment is inhibition of proinflammatory cytokine release.
白细胞介素-10可保护小鼠免受脂多糖诱导的致死作用。为确定白细胞介素-10对脂多糖诱导的炎症反应的影响，对6只东非狒狒静脉注射亚致死剂量的脂多糖（鼠伤寒沙门氏菌；500微克/千克），注射前分别给予人重组白细胞介素-10（n = 3，500微克/千克）或稀释剂（n = 3）。白细胞介素-10强烈抑制脂多糖诱导的肿瘤坏死因子、白细胞介素-6、白细胞介素-8和白细胞介素-12的释放（所有p < 0.05）。相比之下，白细胞介素-10既不影响凝血系统的激活（血浆凝血酶/抗凝血酶III复合物水平），也不影响纤维蛋白溶解系统的激活（血浆组织型纤溶酶原激活剂、I型纤溶酶原激活剂抑制剂和纤溶酶/α2-抗纤溶酶复合物水平）。白细胞介素-10适度减轻中性粒细胞增多和中性粒细胞脱颗粒（血浆弹性蛋白酶/α1-抗胰蛋白酶复合物浓度）（两者p < 0.05）。循环粒细胞表面肿瘤坏死因子受体表达的变化不受白细胞介素-10影响。这些结果表明，在亚致死性内毒素血症期间，白细胞介素-10治疗的主要抗炎作用是抑制促炎细胞因子的释放。
