Ed Rainger G, Chimen Myriam, Harrison Matthew J, Yates Clara M, Harrison Paul, Watson Stephen P, Lordkipanidzé Marie, Nash Gerard B
Centre for Cardiovascular Sciences, Institute for Biomedical Research, The Medical School, The University of Birmingham , Birmingham , UK and.
Platelets. 2015;26(6):507-20. doi: 10.3109/09537104.2015.1064881. Epub 2015 Jul 21.
Besides their role in the formation of thrombus during haemostasis, it is becoming clear that platelets contribute to a number of other processes within the vasculature. Indeed, the integrated function of the thrombotic and inflammatory systems, which results in platelet-mediated recruitment of leukocytes, is now considered to be of great importance in the propagation, progression and pathogenesis of atherosclerotic disease of the arteries. There are three scenarios by which platelets can interact with leukocytes: (1) during haemostasis, when platelets adhere to and are activated on sub-endothelial matrix proteins exposed by vascular damage and then recruit leukocytes to a growing thrombus. (2) Platelets adhere to and are activated on stimulated endothelial cells and then bridge blood borne leukocytes to the vessel wall and. (3) Adhesion between platelets and leukocytes occurs in the blood leading to formation of heterotypic aggregates prior to contact with endothelial cells. In the following review we will not discuss leukocyte recruitment during haemostasis, as this represents a physiological response to tissue trauma that can progress, at least in its early stages, in the absence of inflammation. Rather we will deal with scenarios 2 and 3, as these pathways of platelet-leukocyte interactions are important during inflammation and in chronic inflammatory diseases such as atherosclerosis. Indeed, these interactions mean that leukocytes possess means of adhesion to the vessel wall under conditions that may not normally be permissive of leukocyte-endothelial cell adhesion, meaning that the disease process may be able to bypass the regulatory pathways which would ordinarily moderate the inflammatory response.
除了在止血过程中形成血栓的作用外,越来越清楚的是血小板在脉管系统内的许多其他过程中也发挥作用。事实上,血栓形成系统和炎症系统的整合功能导致血小板介导白细胞的募集,现在被认为在动脉粥样硬化疾病的传播、进展和发病机制中具有重要意义。血小板与白细胞相互作用有三种情况:(1)在止血过程中,血小板黏附于血管损伤暴露的内皮下基质蛋白并被激活,然后将白细胞募集到正在形成的血栓中。(2)血小板黏附于受刺激的内皮细胞并被激活,然后将血源性白细胞连接到血管壁。(3)血小板与白细胞在血液中发生黏附,导致在与内皮细胞接触之前形成异型聚集体。在接下来的综述中,我们将不讨论止血过程中的白细胞募集,因为这代表了对组织创伤的生理反应,至少在其早期阶段,可以在没有炎症的情况下进展。相反,我们将讨论情况2和3,因为这些血小板-白细胞相互作用途径在炎症期间以及在诸如动脉粥样硬化等慢性炎症疾病中很重要。事实上,这些相互作用意味着白细胞在通常不允许白细胞-内皮细胞黏附的条件下具有黏附于血管壁的方式,这意味着疾病过程可能能够绕过通常会调节炎症反应的调节途径。