van der Poll T, Jansen J, Levi M, ten Cate H, Hack C E, Aarden L A, ten Cate J W, van Deventer S J
Department of Internal Medicine, Academic Medical Center, University of Amsterdam, The Netherlands.
Scand J Immunol. 1996 Jan;43(1):122-5. doi: 10.1046/j.1365-3083.1996.d01-12.x.
Interleukin (IL-)10 has been demonstrated to inhibit endotoxin-induced production of a number of pro-inflammatory cytokines. The present study sought to compare the appearances in the circulation of IL-10, IL-6 and IL-8, and to assess the roles of endogenously produced platelet-activating factor (PAF) and IL-6 in IL-10 release during endotoxaemia in chimpanzees. Intravenous injection of endotoxin (lot EC-5, 4 ng/kg, n = 8) induced a transient rise in serum IL-10 concentrations, peaking after 2 h (213 +/- 70 pg/ml; P < 0.05). No correlations existed between peak IL-10 levels, and peak IL-6 and IL-8 levels. Neither infusion of the specific PAF antagonist TCV-309 (n = 4), nor infusion of a neutralizing anti-IL-6 monoclonal antibody (n = 4) influenced endotoxin-induced IL-10 release. IL-10 release elicited by injection of endotoxin is not mediated by PAF or IL6.
白细胞介素(IL-)10已被证明可抑制内毒素诱导的多种促炎细胞因子的产生。本研究旨在比较IL-10、IL-6和IL-8在循环中的表现,并评估内源性产生的血小板活化因子(PAF)和IL-6在黑猩猩内毒素血症期间IL-10释放中的作用。静脉注射内毒素(批号EC-5,4 ng/kg,n = 8)导致血清IL-10浓度短暂升高,2小时后达到峰值(213±70 pg/ml;P < 0.05)。IL-10峰值水平与IL-6和IL-8峰值水平之间不存在相关性。输注特异性PAF拮抗剂TCV-309(n = 4)或中和性抗IL-6单克隆抗体(n = 4)均不影响内毒素诱导的IL-10释放。注射内毒素引发的IL-10释放不是由PAF或IL-6介导的。