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脂多糖引发兔血小板反应的机制:溶解反应对替代补体途径的依赖性

Mechanisms of lipopolysaccharide-initiated rabbit platelet responses: alternative complement pathway dependence of the lytic response.

作者信息

Morrison D C, Kline L F, Oades Z G, Henson P M

出版信息

Infect Immun. 1978 Jun;20(3):744-51. doi: 10.1128/iai.20.3.744-751.1978.

Abstract

Experiments were performed to examine the relationship of endotoxin-initiated complement activation and rabbit platelet lysis. The results of these experiments supported the concept that activation of the alternative pathway is required for endotoxin-initiated complement-dependent rabbit platelet lysis. Our data demonstrated that preparations of endotoxin or isolated lipid A, which activate selectively the classical pathway, are incapable of initiating platelet lysis. Essentially equivalent results were obtained in citrated or heparinized plasma, although the latter anticoagulated plasma appeared to be more efficient in supporting lysis. Additional data support the concept that natural antibody to either the polysaccharide or the lipid A region of the lipopolysaccharide, which might be present in rabbit plasma, probably did not play a prominent role in the complement-mediated lytic response.

摘要

进行了实验以研究内毒素引发的补体激活与兔血小板溶解之间的关系。这些实验结果支持了这样一种概念,即内毒素引发的补体依赖性兔血小板溶解需要替代途径的激活。我们的数据表明,选择性激活经典途径的内毒素制剂或分离的脂多糖A不能引发血小板溶解。在枸橼酸盐或肝素化血浆中获得了基本相同的结果,尽管后者抗凝的血浆似乎在支持溶解方面更有效。其他数据支持这样一种概念,即兔血浆中可能存在的针对脂多糖多糖或脂多糖A区域的天然抗体,可能在补体介导的溶解反应中不起主要作用。

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