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阿司匹林和P2Y12抑制剂在血小板介导的中性粒细胞和单核细胞活化中的作用

Aspirin and P2Y12 Inhibitors in platelet-mediated activation of neutrophils and monocytes.

作者信息

Schrottmaier Waltraud C, Kral Julia B, Badrnya Sigrun, Assinger Alice

机构信息

Dr. Alice Assinger, Centre for Physiology and Pharmacology, Medical University of Vienna, Schwarzspanierstrasse 17, A-1090 Vienna, Austria, Tel.: +43 1 40160 31405, E-mail:

出版信息

Thromb Haemost. 2015 Aug 31;114(3):478-89. doi: 10.1160/TH14-11-0943. Epub 2015 Apr 23.

DOI:10.1160/TH14-11-0943
PMID:25904241
Abstract

Platelets are key players in haemostasis and represent a pivotal link between inflammation, immunity and atherogenesis. Depending on the (patho)physiological environment platelets modulate various leukocyte functions via release of inflammatory mediators and direct cell-cell interactions. Elevated levels of circulating platelet-leukocyte aggregates are found in patients suffering from several thrombotic or inflammatory conditions. Platelet-monocyte and platelet-neutrophil interaction can trigger pro- and anti-inflammatory responses and modulate effector functions of all leukocyte subpopulations. These platelet-mediated immune responses have implications for the progression of cardiovascular diseases and also play a crucial role during infections, cancer, transplantations and other inflammatory diseases of several organs. Antiplatelet therapy including the COX inhibitor aspirin and/or ADP receptor P2Y12 inhibitors such as clopidogrel, prasugrel and ticagrelor are the therapy of choice for various cardiovascular complications. Both aspirin and P2Y12 inhibitors attenuate platelet-leukocyte interactions, thereby also modulating immune responses. This may have beneficial effects in some pathological conditions, while it might be detrimental in others. This review aims to summarise the current knowledge on platelet-leukocyte interactions and the impact of aspirin and P2Y12 inhibition on platelet-mediated immune responses and to give an overview on the effects of antiplatelet therapy on platelet-leukocyte interplay in various diseases.

摘要

血小板是止血过程中的关键参与者,是炎症、免疫和动脉粥样硬化形成之间的重要纽带。根据(病理)生理环境的不同,血小板通过释放炎症介质和直接的细胞间相互作用来调节多种白细胞功能。在患有多种血栓形成或炎症性疾病的患者中,循环血小板 - 白细胞聚集体水平升高。血小板 - 单核细胞和血小板 - 中性粒细胞相互作用可触发促炎和抗炎反应,并调节所有白细胞亚群的效应功能。这些血小板介导的免疫反应对心血管疾病的进展有影响,在感染、癌症、移植及其他多个器官的炎症性疾病中也起着关键作用。抗血小板治疗,包括环氧化酶(COX)抑制剂阿司匹林和/或二磷酸腺苷(ADP)受体P2Y12抑制剂,如氯吡格雷、普拉格雷和替格瑞洛,是治疗各种心血管并发症的首选疗法。阿司匹林和P2Y12抑制剂均可减弱血小板 - 白细胞相互作用,从而也调节免疫反应。这在某些病理状况下可能具有有益作用,而在其他情况下可能有害。本综述旨在总结关于血小板 - 白细胞相互作用的当前知识,以及阿司匹林和P2Y12抑制对血小板介导的免疫反应的影响,并概述抗血小板治疗对各种疾病中血小板 - 白细胞相互作用的作用。

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