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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 investigate the effect of interleukin 10 (IL 10) on the inflammatory response of alveolar macrophages. Methods: Mouse alveolar macrophages cultured in vitro were stimulated with lipopolysaccharide (LPS) and the effects of IL 10 on the release of cytokines by alveolar macrophages were observed. RESULTS: The alveolar macrophages released the highest levels of TNFα, IL-1β and IL-6 at 6, 12 and 24 hours after stimulation with 10 mg / L LPS, with concentrations of (1790 ± 985) ng / L , (986 ± 35 7) ng / L and (42 33 ± 6 57) ng / L, respectively, P <0.05 compared with L PS stimulation. IL-10 increased continuously at 8 hours after LPS stimulation (2 38 ± 87 ng / L) and peaked at 24 hours with a concentration of (16 0 ± 5 2 1) ng / L (P 0 .0 5). The inhibition of endogenous IL 10 release by 15 μg / L IL 10 monoclonal antibody resulted in a significant increase of TNFα, IL 1β and IL 6 release (16 89 ± 36 4 ng / L, (12 000 ± 2 5 3) ng / L and (5269 ± 1127) ng / L. Administration of exogenous recombinant IL-10 (50 μg / L) significantly inhibited LPS-induced release of TNFα, IL-1β and IL-6 by 52%, 84% and 39%, respectively. CONCLUSION: IL 10 has a significant inhibitory effect on the release of inflammatory cytokines. Supplementation of exogenous IL 10 helps to control the abnormal inflammatory response of alveolar macrophages.