Inhibition of the activation of hageman factor (factor XII) by eosinophils and eosinophilic constituents.
Inhibition of the activation of hageman factor (factor XII) by eosinophils and eosinophilic constituents.
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嗜酸性粒细胞和嗜酸性粒细胞成分抑制哈格曼因子（因子 XII）的激活。
DOI：
10.1002/ajh.2830420127
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发表时间：
1993
影响因子：
12.8
通讯作者：
Embury,P
中科院分区：
文献类型：
--
作者：
Ratnoff,OD;Gleich,GJ;Shurin,SB;Kazura,J;Everson,B;Embury,P
一些以显着嗜酸性粒细胞增多为特征的综合征可能因血栓形成而并发。所描述的实验表明，矛盾的是，嗜酸性粒细胞及其某些成分抑制哈格曼因子（HF，因子 XII）的激活。在早期的研究中，混合类型的粒细胞、其他有核外周血细胞和血小板的悬浮液抑制了鞣花酸、玻璃和硫苷脂对哈格曼因子的激活。这些细胞经离心沉淀后，上清液也具有抑制作用。早些时候没有尝试区分不同的粒细胞种类。在本研究中，通过离心分离嗜酸性粒细胞的悬浮液和上清液，鞣花酸抑制了哈格曼因子的激活。抑制活化约一半的上清液的蛋白质浓度为16μg/ml，与对于外周血单核细胞悬浮液所描述的大致相同。鞣花酸对哈格曼因子的激活也受到嗜酸性粒细胞的某些成分的抑制，包括嗜酸性粒细胞过氧化物酶、嗜酸性粒细胞主要碱性蛋白和嗜酸性粒细胞阳离子蛋白。抑制作用对于鞣花酸诱导的哈格曼因子的激活并不具有特异性，因为在硫苷脂诱导的激活中也观察到了抑制作用。抑制作用可能与哈格曼因子激活剂负电荷的中和有关。因此，次没食子酸铋（一种哈格曼因子的颗粒激活剂）在暴露于嗜酸性粒细胞阳离子蛋白后不再有效。这里报告的观察结果提出了体内嗜酸性粒细胞是否调节归因于哈格曼因子的某些防御反应的问题。 © 1993 Wiley-Liss, Inc.
Several syndromes characterized by striking eosinophilia may be complicated by thrombosis. The experiments described indicate that, paradoxically, eosinophils and certain of their constituents inhibit the activation of Hageman factor (HF, factor XII). In earlier studies, suspensions of mixed types of granulocytes, other nucleated peripheral blood cells, and platelets inhibited activation of Hageman factor by ellagic acid, glass, and sulfatides. After these cells were sedimented by centrifugation, the supernatant fluids were also inhibitory. No attempt had been made earlier to distinguish among different granulocytic species. In the present study, suspensions of eosinophils and the supernatant fluid after eosinophils had been separated by centrifugation inhibited activation of Hageman factor by ellagic acid. The protein concentration of that amount of supernatant fluid that inhibited activation by about half was 16 μg/ml, approximately the same as had been described for suspensions of peripheral blood mononuclear cells. Activation of Hageman factor by ellagic acid was also inhibited by certain constituents of eosinophils, including eosinophil peroxidase, eosinophil major basic protein and eosinophil cationic protein. Inhibition was not specific for ellagic acid‐induced activation of Hageman factor, as inhibition was also observed with sulfatide‐induced activation. Inhibition was presumably related to neutralization of the negative charge of activators of Hageman factor. Thus, bismuth subgallate, a particulate activator of Hageman factor, was no longer effective after it had been exposed to eosinophil cationic protein. The observations reported here raise the question of whether in vivo eosinophils modulate certain of the defense reactions ascribed to Hageman factor. © 1993 Wiley‐Liss, Inc.