血小板活化因子（PAF）在钩端螺旋体脂多糖刺激后细胞反应中的作用。

Role of platelet-activating-factor (PAF) on cellular responses after stimulation with leptospire lipopolysaccharide.

作者信息

Isogai E, Hirose K, Kimura K, Hayashi S, Kubota T, Fujii N, Isogai H

机构信息

Department of Preventive Dentistry, Health Sciences University of Hokkaido, Japan.

出版信息

Microbiol Immunol. 1997;41(3):271-5. doi: 10.1111/j.1348-0421.1997.tb01200.x.

DOI:10.1111/j.1348-0421.1997.tb01200.x

PMID:9130240

Abstract

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.

摘要

钩端螺旋体脂多糖（LPS）刺激多形核中性粒细胞（PMN）黏附于人脐静脉内皮细胞（HUVEC）。对钩端螺旋体LPS的反应中PMN黏附增强可由血小板激活因子（PAF）介导，因为PAF拮抗剂可降低黏附。钩端螺旋体LPS还诱导血小板或U937黏附。第二个实验涉及钩端螺旋体LPS在PMN-血小板混合物中引发血小板聚集，因为钩端螺旋体LPS刺激人PMN而非人血小板。血小板反应仅在混合系统中观察到，并被PAF拮抗剂抑制。PAF可能是人类钩端螺旋体病的一个重要致病因素。