白介素-10对肺泡巨噬细胞致炎效应的调节作用  

Effect of interleukin10 on inflammatory response by alveolar macrophages in mice

作　　者：邱海波[1] 周韶霞[1] 陈德昌[2] 

机构地区：[1]东南大学医学院第一附属医院ICU,江苏南京210009 [2]中国医学科学院中国协和医科大学北京协和医院ICU,北京100730

出　　处：《中国危重病急救医学》2000年第6期353-355,共3页Chinese Critical Care Medicine

基　　金：江苏省青年基金!资助项目 ( BQ980 3 5 )

摘　　要：目的 :探讨白介素 10 (IL 10 )对肺泡巨噬细胞致炎效应的影响。方法 :内毒素 (L PS)刺激体外培养的小鼠肺泡巨噬细胞 ,观察 IL 10对肺泡巨噬细胞释放细胞因子的影响。结果 :肺泡巨噬细胞受 10 mg/LL PS刺激后 6、12和 2 4小时 ,肿瘤坏死因子α(TNFα)、IL 1β和 IL 6释放达峰值 ,浓度分别为 (1790±985 ) ng/L、(986± 35 7) ng/L 和 (42 33± 6 5 7) ng/L,与 L PS刺激 0时比较 ,P均 <0 .0 5。IL 10在 L PS刺激后 8小时持续升高〔(2 38± 87) ng/L〕,2 4小时达到峰值 ,浓度为 (16 0 0± 5 2 1) ng/L(P<0 .0 5 )。 15 0 μg/L IL 10单克隆抗体抑制内源性 IL 10释放后 ,导致 TNFα、IL 1β、IL 6释放明显增加 ,分别达 (16 89± 36 4) ng/L、(12 0 0± 2 5 3) ng/L 和 (5 2 6 9± 112 7) ng/L。给予外源性重组 IL 10 (5 0 μg/L) ,则明显抑制 L PS诱导的TNFα、IL 1β、IL 6释放 ,浓度分别降低 5 2 %、84%和 39%。结论 :IL 10对炎症性细胞因子释放具有明显抑制作用 ,补充外源性 IL 10有助于控制肺泡巨噬细胞的异常炎症反应。Objective:To observe the regulatory effect of interleukin10(IL10) on inflammatory response by alveolar macrophages.Methods:Alveolar macrophages from mice were isolated and incubated with endotoxin.IL1β,IL6,and IL10 levels were measured by enzymelinked immunosorbent assay(ELISA).Results:After endotoxin stimulation,TNFα,IL1β,IL6,and IL10 levels peaked at 6,12,24,and 24 hours in alveolar macrophages respectively,peak concentration of these cytokines were (1 790±985)ng/L,(986± 357)ng/L ,(4 233±657)ng/L,and (1 600±521)ng/L (all P <0 05).Treatment with monoclonal antibody against IL10 (150 μg/L) could significantly neutralize endogenous IL10 release,and markedly enhance formation of TNFα,IL1β and IL6〔(1 689±364)ng/L,(1 200±253)ng/L and (5 269±1 127)ng/L〕.However,TNFα,IL1β and IL6 secretion were inhibited by recombinant IL10 (50 μg/L),the concentration of the cytokines decreased by 52%,84% and 39% respectively.Conclusions:Endogenous and exogenous IL10 can inhibit the endotoxininduced inflammatory cytokine secretion in alveolar macrophages.

关 键 词：肺泡巨噬细胞 炎症反应 呼吸窘迫 IL-10 TNF-Α 

分 类 号：R363[医药卫生—病理学]