de Stoppelaar Sacha F, van 't Veer Cornelis, van der Poll Tom
Sacha F. de Stoppelaar, MD, Academic Medical Centre, Centre of Experimental and Molecular Medicine, Meibergdreef 9, Room G2-130, 1105 AZ Amsterdam, the Netherlands, Tel.: +31 20 5665910, Fax: +31 20 6977192, E-mail:
Thromb Haemost. 2014 Oct;112(4):666-77. doi: 10.1160/TH14-02-0126. Epub 2014 Jun 26.
Platelets are small circulating anucleate cells that are of crucial importance in haemostasis. Over the last decade, it has become increasingly clear that platelets play an important role in inflammation and can influence both innate and adaptive immunity. Sepsis is a potentially lethal condition caused by detrimental host response to an invading pathogen. Dysbalanced immune response and activation of the coagulation system during sepsis are fundamental events leading to sepsis complications and organ failure. Platelets, being major effector cells in both haemostasis and inflammation, are involved in sepsis pathogenesis and contribute to sepsis complications. Platelets catalyse the development of hyperinflammation, disseminated intravascular coagulation and microthrombosis, and subsequently contribute to multiple organ failure. Inappropriate accumulation and activity of platelets are key events in the development of sepsis-related complications such as acute lung injury and acute kidney injury. Platelet activation readouts could serve as biomarkers for early sepsis recognition; inhibition of platelets in septic patients seems like an important target for immune-modulating therapy and appears promising based on animal models and retrospective human studies.
血小板是循环系统中的无核小细胞，在止血过程中至关重要。在过去十年中，越来越清楚的是血小板在炎症中发挥重要作用，并且可以影响固有免疫和适应性免疫。脓毒症是由宿主对入侵病原体的有害反应引起的潜在致命病症。脓毒症期间免疫反应失衡和凝血系统激活是导致脓毒症并发症和器官衰竭的基本事件。血小板作为止血和炎症中的主要效应细胞，参与脓毒症发病机制并导致脓毒症并发症。血小板催化过度炎症、弥散性血管内凝血和微血栓形成的发展，随后导致多器官衰竭。血小板的不适当聚集和活性是脓毒症相关并发症如急性肺损伤和急性肾损伤发生发展的关键事件。血小板激活读数可作为早期脓毒症识别的生物标志物；基于动物模型和回顾性人体研究，抑制脓毒症患者的血小板似乎是免疫调节治疗的一个重要靶点，并且前景乐观。
