Release of platelet-activating factor in human pathology. I. Evidence for the occurrence of basophil degranulation and release of platelet-activating factor in systemic lupus erythematosus.
Release of platelet-activating factor in human pathology. I. Evidence for the occurrence of basophil degranulation and release of platelet-activating factor in systemic lupus erythematosus.
复制标题
人类病理学中血小板激活因子的释放。
DOI：
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发表时间：
1981
期刊：
影响因子：
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通讯作者：
J. Benveniste
中科院分区：
文献类型：
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作者：
G. Camussi;C. Tetta;R. Coda;J. Benveniste
在兔急性血清病中，嗜碱性粒细胞脱颗粒和血小板活化因子（PAF acether）的释放与血管通透性增加和免疫复合物沉积有关。PAF-乙酸酯是过敏反应的磷脂介质，从包括人在内的几种哺乳动物的白细胞中释放，聚集血小板并释放其血管活性胺。在这篇文章中，我们评估了系统性红斑狼疮患者嗜碱性粒细胞脱颗粒和PAF-乙酸释放的发生。在疾病的急性期，嗜碱性粒细胞在体内脱颗粒，从白细胞释放的PAF-乙酸的量显着减少。在缓解期或疾病的潜伏期，异染性嗜碱性粒细胞数量增加。在体外，DNA攻击后，观察到颗粒的脱颗粒和PAF-乙酸酯的释放。电子显微镜研究表明，嗜碱性粒细胞确实脱颗粒DNA的反应。这些研究还表明，即使人血小板聚集的其他两种途径，即，ADP和花生四烯酸依赖性途径被阻断。嗜碱性粒细胞的脱粒和PAF-乙酰基醚的释放，以及脱粒嗜碱性粒细胞和聚集的血小板之间的相互作用的形态学证据的伴随，强烈提示PAF-乙酰基醚从系统性红斑狼疮嗜碱性粒细胞的释放。
Basophil degranulation and release of platelet-activating factor (PAF acether) have been implicated in enhanced vascular permeability and immune complex deposition in rabbit acute serum sickness. PAF-acether is a phospholipid mediator of anaphylaxis, released from leukocytes of several mammalian species, including man, that aggregates platelets and releases their vasoactive amines. In this article, we evaluated the occurrence of basophil degranulation and release of PAF-acether in patients with systemic lupus erythematosus. In the acute phases of the disease, basophils were in vivo degranulated, and the amount of PAF-acether releasable from leukocytes was markedly reduced. During remission or in the latent phases of the disease, when the number of metachromatically staining basophils increased. in an vitro degranulation and release of PAF-acether were observed after DNA challenge. Electron microscopy studies demonstrated that basophils indeed degranulated in response to DNA. These studies also showed the interaction between degranulating basophils and human platelets which aggregated even if the other two pathways of human platelet aggregation, i.e., the ADP- and the arachidonic acid-dependent pathways, were blocked. The concomitance of basophil degranulation and release of PAF-acether, together with the morphologic evidence of the interaction between degranulating basophils and aggregated platelets, was strongly suggestive of release of PAF-acether from basophils in systemic lupus erythematosus.