Role of platelet-activating-factor (PAF) on cellular responses after stimulation with leptospire lipopolysaccharide
Role of platelet-activating-factor (PAF) on cellular responses after stimulation with leptospire lipopolysaccharide
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DOI：
10.1111/j.1348-0421.1997.tb01200.x
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发表时间：
1997-01-01
影响因子：
2.6
通讯作者：
Isogai, H
中科院分区：
文献类型：
--
作者：
Isogai, E;Hirose, K;Isogai, H
钩端螺旋体脂多糖（LPS）刺激多形核中性粒细胞（PMNs）与人脐静脉内皮细胞（HUVEC）粘附。血小板激活因子（PAF）可介导钩端螺旋体LPS引起的PMN粘附增强，因为PAF拮抗剂可降低粘附。钩端螺旋体LPS也诱导血小板或U937粘附。第二个实验涉及钩端螺旋体LPS在PMN-血小板混合物中引起血小板聚集，因为钩端螺旋体LPS刺激人PMN但不刺激人血小板。血小板反应仅在混合体系中观察到，并被PAF拮抗剂抑制。PAF可能是钩端螺旋体病的重要致病因子。
Leptospire lipopolysaccharide (LPS) stimulated the adherence of polymorphonuclear neutrophils (PMNs) to human umbilical vein endothelial cells (HUVEC). Enhanced PMN adherence in response to leptospire LPS can be mediated by platelet-activator-factor (PAF), because a PAF antagonist reduced adherence. Leptospire LPS also induced the adherence platelets or U937. The second experiment involved leptospire LPS elicited platelet aggregation in a PMN-platelet mixture, because leptospire LPS stimulated human PMN but not the human platelets. The platelet response was observed only in the mixture system and was inhibited by a PAF antagonist. PAF could be an important pathogenic factor in human leptospirosis.