摘要
本研究旨在观察IL 10对肺泡巨噬细胞 (AM)、清道夫受体 (SR)、CD14表达的影响 ,探讨IL 10在内毒素血症时防止AM由免疫防御向炎症效应转变中的作用。分离培养小鼠AM ,以不同剂量 (0 ,0 0 1,0 1,1,10 ,10 0 μg/L)IL 10刺激细胞 16h或以 10 0 μg/LIL 10刺激细胞不同时间 (0 ,2 ,4 ,6 ,8,12 ,16h) ,采用免疫细胞化学及RT PCR方法观察SR、CD14表达变化。结果显示低至 10 μg/LIL 10刺激 16h或 10 0 μg/LIL 10刺激 12～ 2 4h能显著增强SRmRNA并抑制CD14mRNA表达 ,SR蛋白表达也显著增强 ,但CD14蛋白表达无明显变化。IL 10刺激下对SR蛋白表达的增强能降低AM对LPS的反应性 。
To study the effects of IL 10 on expression of CD14 and scavenger receptor (SR) in alveolar macrophages (AM). AM were incubated with different dose (0, 0.01,0.1,1,10,100 μg/L) of IL 10 for 16 hours(h) or with 100 μg/L IL 10 for different time span(0,2,4,6, 8,12,16h). Immunocytochemistry and RT PCR were used to detect the expression of SR and CD14 on both protein and mRNA levels. SRmRNA expression was enhanced and CD14mRNA expression was inhibited when AM were stimulated by IL 10 with 10μg/L or higher concentrations for 16h or with 100μg/L IL 10 for 12～24h. SR protein expression, but not CD14, was significantly up regulated at the same time. The results suggested that IL 10 prevented AM to shift to inflammatory mediators during endotoximia by enhancing the SR protein expression.
出处
《基础医学与临床》
CSCD
北大核心
2003年第1期44-47,共4页
Basic and Clinical Medicine
基金
国家重点基础研究发展规划 (G19990 5 4 2 0 0 )
国家自然科学基金 (39870 313)
军队杰出中青年科学基金
