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Platelet – Leukocyte Interactions: Multiple Links Between Inflammation Blood Coagulation and Vascular Risk

机译:血小板-白细胞相互作用:炎症凝血和血管风险之间的多重联系

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摘要

The aim of this review is to summarize the contribution of platelets and leukocytes and their interactions in inflammation and blood coagulation and its possible relevance in the pathogenesis of thrombosis. There is some evidence of an association between infection/inflammation and thrombosis. This is likely a bidirectional relationship. The presence of a thrombus may serve as a nidus of infection. Vascular injury indeed promotes platelet and leukocyte activation and thrombus formation and the thrombus and its components facilitate adherence of bacteria to the vessel wall. Alternatively, an infection and the associated inflammation can trigger platelet and leukocyte activation and thrombus formation. In either case platelets and leukocytes co-localize and interact in the area of vascular injury, at sites of inflammation and/or at sites of thrombosis. Following vascular injury, the subendothelial tissue, a thrombogenic surface, becomes available for interaction with these blood cells. Tissue factor, found not only in media and adventitia of the vascular wall, but also on activated platelets and leukocytes, triggers blood coagulation. Vascular-blood cell interactions, mediated by the release of preformed components of the endothelium, is modulated by both cell adhesion and production of soluble stimulatory or inhibitory molecules that alter cell function: adhesion molecules regulate cell-cell contact and facilitate the modulation of biochemical pathways relevant to inflammatory and/or thrombotic processes.
机译:这篇综述的目的是总结血小板和白细胞的作用及其在炎症和凝血中的相互作用,以及它们与血栓形成的可能相关性。有证据表明感染/炎症与血栓形成之间存在关联。这可能是双向关系。血栓的存在可能会导致感染。血管损伤的确促进了血小板和白细胞的活化以及血栓的形成,血栓及其成分促进了细菌粘附在血管壁上。或者,感染和相关的炎症可触发血小板和白细胞活化以及血栓形成。在任一种情况下,血小板和白细胞在血管损伤区域,炎症部位和/或血栓形成部位共定位并相互作用。血管损伤后,可形成血栓形成表面的内皮下组织可与这些血细胞相互作用。不仅存在于血管壁的中膜和外膜中,而且存在于活化的血小板和白细胞中的组织因子都会触发血液凝固。内皮细胞预先形成的成分的释放介导的血管-血液细胞相互作用受到细胞粘附和改变细胞功能的可溶性刺激或抑制分子产生的调节:粘附分子调节细胞与细胞的接触并促进生化途径的调节与炎症和/或血栓形成过程有关。

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