Australian Centre for Blood Diseases, Monash University, Melbourne, Australia.
Thromb Res. 2013 Mar;131(3):191-7. doi: 10.1016/j.thromres.2012.11.028. Epub 2012 Dec 20.
Platelet activation is known to be associated with the release of a vast array of chemokines and proinflammatory lipids which induce pleiotropic effects on a wide variety of tissues and cells, including leukocytes. During thrombosis, the recruitment of leukocytes to activated platelets is considered an important step which not only links thrombosis to inflammatory responses but may also enhance procoagulant state. This phenomenon is highly regulated and influenced by precise mutual interactions between the cells at site of vascular injury and thrombi formation. Platelet-leukocyte interaction involves a variety of mediators including adhesion molecules, chemokines and chemoattractant molecules, shed proteins, various proinflammatory lipids and other materials. The current review addresses the detailed mechanisms underlying platelet-leukocyte crosstalk. This includes their adhesive interactions, transcellular metabolisms, induced tissue factor activity and neutrophil extracellular traps formation as well as the impacts of these phenomena in modulation of the proinflammatory and procoagulant functions in a reciprocal manner that enhances the physiological responses.
血小板激活被认为与大量趋化因子和促炎脂质的释放有关，这些趋化因子和促炎脂质对包括白细胞在内的各种组织和细胞产生多效性作用。在血栓形成过程中，白细胞向激活的血小板募集被认为是一个重要步骤，它不仅将血栓形成与炎症反应联系起来，而且可能增强促凝状态。这种现象受到高度调控，并受到血管损伤和血栓形成部位细胞之间精确相互作用的影响。血小板-白细胞相互作用涉及多种介质，包括粘附分子、趋化因子和趋化因子样分子、脱落蛋白、各种促炎脂质和其他物质。本综述探讨了血小板-白细胞相互作用的详细机制。这包括它们的粘附相互作用、跨细胞代谢、诱导的组织因子活性和中性粒细胞细胞外陷阱的形成，以及这些现象在相互调节促炎和促凝功能方面的影响，增强了生理反应。
