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目的 比较类风湿关节炎 (rheumatoidarthritis,RA)、骨关节炎 (osteoarthritis ,OA)和创伤后手术(post traumatic ,PT)患者滑膜细胞产生巨噬细胞炎症蛋白 1 α(MIP 1α)、MIP 1β和活化正常T细胞表达和分泌调节因子 (RANTES)的差异 ,探讨MIP 1α在体外能否诱导RA滑膜成纤维细胞增殖反应。方法 收集RA、OA和PT患者滑膜组织。采用胶原酶消化法获得滑膜细胞 ,采用组织块贴壁法获得滑膜成纤维细胞。滑膜细胞培养上清中MIP 1α、MIP 1β和RANTES检测采用ELISA法。滑膜成纤维细胞增殖反应采用四甲基偶氮唑盐微量酶反应比色法 (MTT法 )。结果 RA、OA和PT患者的滑膜细胞在体外不能自发产生MIP 1α、MIP 1β和RANTES。用LPS(5 μg/ml)和白介素 1α(rhIL 1α ,5 0U/ml)刺激滑膜细胞后 ,RA患者滑膜细胞可产生较高的MIP 1α和RANTES ,并明显多于OA和PT患者滑膜细胞产生的量 ,而滑膜细胞产生MIP 1β量在 3种类型患者中无明显差异。MIP 1α可诱导RA滑膜成纤维细胞增殖反应 ,并且在一定浓度范围内 (2～ 5 0ng/ml)具有浓度依赖性。结论 RA滑膜细胞在体外产生MIP 1α和RANTES的量明显高于OA和PT患者 ,MIP 1α诱导RA滑膜成纤维细胞的增殖反应。提示MIP 1α在RA的发病机制中可能起重要作用。
Objective To compare the expression of MIP 1α (MIP 1α), MIP 1β and synovial fluid in synovial cells of rheumatoid arthritis (RA), osteoarthritis (OA) and post traumatic (PT) Activation of normal T cells and secretion of regulatory factors (RANTES) differences to explore MIP 1α in vitro can induce RA synovial fibroblasts proliferation reaction. Methods The synovial tissues of patients with RA, OA and PT were collected. Synovial cells were obtained by collagenase digestion, and synovial fibroblasts were obtained by tissue block method. Synovial cell culture supernatants MIP 1α, MIP 1β and RANTES detection using ELISA method. Synovial fibroblast proliferation reaction using tetramethylazizoles trace enzyme reaction colorimetry (MTT method). Results Synoviocytes from patients with RA, OA and PT did not spontaneously produce MIP 1α, MIP 1β and RANTES in vitro. Synovial cells of RA patients produced higher MIP 1α and RANTES after stimulation with LPS (5 μg / ml) and interleukin-1α (rhIL 1α, 50 U / ml) than those with OA and PT Membrane-derived cells, whereas the amount of MIP 1β produced by synovial cells showed no significant difference among the three types of patients. MIP 1α induced RA synovial fibroblast proliferation response in a concentration range (2 ~ 50ng / ml) with a concentration-dependent manner. Conclusions The amount of MIP 1α and RANTES produced by RA synovial cells in vitro is significantly higher than that in OA and PT patients. MIP 1α induces proliferation of RA synovial fibroblasts. It is suggested that MIP 1α may play an important role in the pathogenesis of RA.