Effects of IL-10 on systemic inflammatory responses during sublethal primate endotoxemia.
Effects of IL-10 on systemic inflammatory responses during sublethal primate endotoxemia.
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DOI：
10.4049/jimmunol.158.4.1971
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发表时间：
1997-02
影响因子：
4.4
通讯作者：
T. Pollvander;P. Jansen;W. Montegut;Carla C. Braxton;S. Calvano;S. A. Stackpole;Sean Smith;S. Swanson;C. Hack;Stephen F. Lowry;L. Moldawer
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作者：
T. Pollvander;P. Jansen;W. Montegut;Carla C. Braxton;S. Calvano;S. A. Stackpole;Sean Smith;S. Swanson;C. Hack;Stephen F. Lowry;L. Moldawer
IL-10保护小鼠免于LPS诱导的致死。为了确定IL-10对LPS诱导的炎症反应的作用，在直接注射人rIL-10（n = 3，500 μ g/kg）或稀释剂（n = 3）之前，静脉内注射亚致死剂量的LPS（鼠伤寒沙门氏菌; 500 μ g/kg）。IL-10强烈抑制LPS诱导的TNF、IL-6、IL-8和IL-12的释放（所有p < 0.05）。相比之下，IL-10既不影响凝血系统的激活（凝血酶/抗凝血酶III复合物的血浆水平），也不影响纤溶系统的激活（组织型纤溶酶原激活物、纤溶酶原激活物抑制剂I型和纤溶酶/α 2-抗纤溶酶复合物的血浆水平）。IL-10适度减弱嗜中性白细胞增多和中性粒细胞脱粒（弹性蛋白酶/α 1-抗胰蛋白酶复合物的血浆浓度）（均p < 0.05）。循环粒细胞表面TNF受体表达的变化不受IL-10的影响。这些结果表明，在亚致死性内毒素血症期间，IL-10治疗的主要抗炎作用是抑制促炎细胞因子释放。
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.