Sheng W S, Hu S, Kravitz F H, Peterson P K, Chao C C
Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, Minnesota 55404, USA.
Clin Diagn Lab Immunol. 1995 Sep;2(5):604-8. doi: 10.1128/cdli.2.5.604-608.1995.
Interleukin (IL)-10 appears to play an important regulatory role in the systemic inflammatory response; however, production of IL-10 within the human central nervous system has not been described. Using cultures of human fetal microglial cells, the resident macrophages of the brain, we investigated the production and regulation of bioactive IL-10. Lipopolysaccharide stimulated acute release of tumor necrosis factor (TNF)-alpha (peak by 8 h) and delayed production of IL-10 (over a 48-h period) in microglial cell cultures. Treatment of microglial cell cultures with TNF-alpha and IL-6 resulted in a dose-dependent release of IL-10. These cytokines also induced expression of IL-10 mRNA. Treatment of microglial cell cultures with IL-10 markedly inhibited TNF-alpha and IL-6 production. These findings suggest that during inflammation within the brain, acute release of TNF-alpha and IL-6 by activated microglia could promote subsequent release of IL-10, which functions to minimize the potential neurotoxic effects of proinflammatory cytokines.
白细胞介素（IL）-10似乎在全身炎症反应中发挥重要调节作用；然而，人类中枢神经系统内IL-10的产生尚未见报道。利用人类胎儿小胶质细胞（大脑中的常驻巨噬细胞）培养物，我们研究了生物活性IL-10的产生及调节。脂多糖刺激小胶质细胞培养物中肿瘤坏死因子（TNF）-α的急性释放（8小时达到峰值）以及IL-10的延迟产生（在48小时内）。用TNF-α和IL-6处理小胶质细胞培养物导致IL-10呈剂量依赖性释放。这些细胞因子还诱导IL-10 mRNA的表达。用IL-10处理小胶质细胞培养物显著抑制TNF-α和IL-6的产生。这些发现表明，在脑部炎症期间，活化的小胶质细胞急性释放TNF-α和IL-6可促进随后IL-10的释放，IL-10的作用是将促炎细胞因子的潜在神经毒性作用降至最低。
