Hashimoto Y, Ziff M, Hurd E R
Arthritis Rheum. 1982 Dec;25(12):1409-18. doi: 10.1002/art.1780251204.
The ability of sera from patients with systemic lupus erythematosus (SLE) and Felty's syndrome to induce increased adhesiveness of normal human neutrophils (PMN) was investigated. PMN from normal healthy donors were incubated in sera from 19 patients with active SLE, 12 with inactive SLE, 20 with Felty's, 24 with rheumatoid arthritis, and 34 normal persons. After incubation, the degree of adherence of the PMN to human endothelial cells in culture, their aggregation, and superoxide (O2-) generation were determined. Sera from patients with both active SLE and Felty's syndrome induced significantly increased PMN adherence to endothelial cells and PMN aggregation in vitro, compared with normal sera. This increased adherence to endothelial cells was maintained after heat treatment (56 degrees C for 30 minutes) of the sera. In O2- generation experiments, sera from patients with active SLE induced significantly increased O2- release from normal PMN using both fresh and heat-treated sera. Sera from Felty's patients demonstrated the same effect with heat-treated sera but not ith fresh sera. When sera from patients with active SLE and Felty's syndrome were used, all three parameters correlated significantly with each other in individual patients. In contrast, sera from the 12 patients with inactive SLE and 24 rheumatoid arthritis patients without Felty's failed to induce significant differences in the three parameters studied when compared with 34 normal controls. Fractionation of 3 SLE sera and 1 Felty's serum on Sephadex G-200 demonstrated that the adherence enhancing factor was present in both IgG and IgG-excluded fractions. The observed increased adhesiveness of PMN induced by SLE and Felty's sera may, at least in part, contribute to the neutropenia which is common in these diseases. Increased O2- release associated with PMN adherence may contribute to endothelial cell damage and vascular injury, which is also a common manifestation of these diseases.
研究了系统性红斑狼疮（SLE）患者和费尔蒂综合征患者的血清诱导正常人中性粒细胞（PMN）黏附性增加的能力。将正常健康供者的PMN与19例活动期SLE患者、12例非活动期SLE患者、20例费尔蒂综合征患者、24例类风湿关节炎患者及34例正常人的血清一起孵育。孵育后，测定PMN对培养的人内皮细胞的黏附程度、其聚集情况以及超氧化物（O2-）的生成。与正常血清相比，活动期SLE患者和费尔蒂综合征患者的血清在体外均显著诱导PMN对内皮细胞的黏附增加及PMN聚集。血清经热处理（56℃ 30分钟）后，对内皮细胞的这种增加的黏附性仍保持。在O2-生成实验中，活动期SLE患者的血清无论是新鲜血清还是热处理血清，均显著诱导正常PMN释放更多的O2-。费尔蒂综合征患者的血清经热处理血清时表现出相同的效果，但新鲜血清则不然。当使用活动期SLE患者和费尔蒂综合征患者的血清时，在个体患者中所有这三个参数彼此显著相关。相比之下，12例非活动期SLE患者及24例无费尔蒂综合征的类风湿关节炎患者的血清与34例正常对照相比，在所研究的三个参数上未诱导出显著差异。用葡聚糖凝胶G - 200对3份SLE血清和1份费尔蒂综合征血清进行分级分离表明，黏附增强因子存在于IgG及IgG排除级分中。观察到SLE和费尔蒂综合征血清诱导的PMN黏附性增加可能至少部分导致了这些疾病中常见的中性粒细胞减少。与PMN黏附相关的O2-释放增加可能导致内皮细胞损伤和血管损伤，这也是这些疾病的常见表现。
