Starkebaum G, Stevens D L, Henry C, Gavin S E
J Lab Clin Med. 1981 Aug;98(2):280-91.
Activation of the neutrophil surface membrane may occur with a variety of stimuli, leading to enhanced glucose oxidation via the hexose monophosphate shunt and production of toxic oxygen radicals such as superoxide anion. This metabolic stimulation may be accompanied by light emission or chemiluminescence. The objective of these studies was to determine the effects of soluble and insoluble immune complexes, IgG aggregates, and rabbit anti-neutrophil serum on neutrophil activation as measured by chemiluminescence. Also, the uptake of immune complexes by neutrophils was determined and was correlated with the solubility of the complexes and the levels of induced chemiluminescence. The results indicate that stimulation of neutrophil chemiluminescence and uptake of immune complexes by neutrophils were both closely correlated with the percent precipitation of the immune complexes. Insoluble immune complexes that were avidly ingested by neutrophils also stimulated maximum levels of chemiluminescence. Nevertheless, elevated levels of chemiluminescence were induced by soluble immune complexes that were poorly ingested by neutrophils. Similarly, soluble aggregated IgG induced elevated levels of neutrophil chemiluminescence in a dose-dependent manner. Aggregated IgG induced up to sixfold higher levels of neutrophil chemiluminescence than did equal amounts of monomeric IgG. Finally, rabbit anti-neutrophil serum also caused increased levels of neutrophil chemiluminescence. Since previous studies have shown that sera from some patients with rheumatoid arthritis and Felty's syndrome have increased amounts of neutrophil-binding IgG due to the presence of both immune complexes and neutrophil-reactive antibodies, the effect of these sera on neutrophil chemiluminescence was studied. Positive correlations were observed between the level of neutrophil chemiluminescence induced by the sera and the amount of serum IgG neutrophil-binding activity (r = 0.72, p less than 0.001) as well as the level of immune complexes determined by C1q binding (r = 0.76, p less than or equal to 0.001). Such neutrophil activation by immune complexes or antibodies may reflect production of toxic oxygen radicals and could subsequently affect neutrophil function.
中性粒细胞表面膜的激活可由多种刺激引发，进而通过磷酸己糖旁路增强葡萄糖氧化，并产生诸如超氧阴离子等有毒氧自由基。这种代谢刺激可能伴有发光或化学发光现象。这些研究的目的是通过化学发光法测定可溶性和不溶性免疫复合物、IgG聚集体以及兔抗中性粒细胞血清对中性粒细胞激活的影响。此外，还测定了中性粒细胞对免疫复合物的摄取情况，并将其与复合物的溶解度及诱导化学发光水平相关联。结果表明，中性粒细胞化学发光的刺激以及中性粒细胞对免疫复合物的摄取均与免疫复合物的沉淀百分比密切相关。被中性粒细胞 avidly摄取的不溶性免疫复合物也能刺激产生最大水平的化学发光。然而，被中性粒细胞摄取较少的可溶性免疫复合物也能诱导化学发光水平升高。同样，可溶性聚集IgG以剂量依赖方式诱导中性粒细胞化学发光水平升高。聚集IgG诱导的中性粒细胞化学发光水平比等量单体IgG高出多达六倍。最后，兔抗中性粒细胞血清也导致中性粒细胞化学发光水平升高。由于先前的研究表明，一些类风湿性关节炎和费尔蒂综合征患者的血清中，由于存在免疫复合物和中性粒细胞反应性抗体，中性粒细胞结合IgG的量增加，因此研究了这些血清对中性粒细胞化学发光的影响。观察到血清诱导的中性粒细胞化学发光水平与血清IgG中性粒细胞结合活性水平（r = 0.72，p小于0.001）以及通过C1q结合测定的免疫复合物水平（r = 0.76，p小于或等于0.001）之间存在正相关。免疫复合物或抗体对中性粒细胞的这种激活可能反映了有毒氧自由基的产生，并可能随后影响中性粒细胞功能。
