Czarnetzki B M, König W, Lichtenstein L M
Int Arch Allergy Appl Immunol. 1978;56(5):398-408.
A low molecular weight eosinophil chemotactic factor (ECF) can be released from human peripheral polymorphonuclear leukocytes by phagocytosis, by reverse anaphylaxis or by the calcium ionophore A 23187. During later phases of ECF-release, a leukocyte-derived ECF inhibitor (LDI) is concomitantly released. Inhibitory activity is also present in sonicates of unstimulated cells, suggesting that the factor is preformed. On chromatographic analysis of neutrophil (PMN) sonicates, two peaks of inhibitory activity at greater than 200,000 and at about 80,000 daltons each are eluted. With preparations containing lymphocytes, monocytes and basophils (L/M/B), only peak (greater than 200,000 daltons) is apparent. The LDI is heat stabile (56 degrees C, 1 h), affects only the ECF and not the migrating eosinophils, and does not inactive bacterial factor or deactivate neutrophils. Evidence is presented suggesting that the mode is by binding of ECF rather than by enzymatic destruction.
一种低分子量嗜酸性粒细胞趋化因子(ECF)可通过吞噬作用、反向过敏反应或钙离子载体A 23187从人外周多形核白细胞中释放出来。在ECF释放的后期,一种白细胞源性ECF抑制剂(LDI)会同时释放出来。未受刺激细胞的超声裂解物中也存在抑制活性,这表明该因子是预先形成的。对中性粒细胞(PMN)超声裂解物进行色谱分析时,分别洗脱了两个抑制活性峰,一个大于200,000道尔顿,另一个约为80,000道尔顿。对于含有淋巴细胞、单核细胞和嗜碱性粒细胞(L/M/B)的制剂,只有大于200,000道尔顿的峰是明显的。LDI对热稳定(56℃,1小时),仅影响ECF而不影响迁移的嗜酸性粒细胞,并且不会使细菌因子失活或使中性粒细胞失活。有证据表明其作用方式是通过与ECF结合而不是酶促破坏。