Leukocytes and platelets must adhere to the wall of blood vessels to carry out their protective functions in inflammation and haemostasis. Recruitment is critically dependent on rheological variables (wall shear rate and stress, red cell aggregation and haematocrit) which affect delivery to the vessel wall as well as velocities and forces experienced there. Leukocyte recruitment is efficient only up to wall shear rates of about 300 s−1 and usually restricted to low-shear post-capillary venules in inflammation. Being smaller, platelets experience lower velocities and shear forces adjacent to the wall and can adhere at much higher shear rates for haemostasis in arteries. In addition, we found quite different effects of variations in haematocrit or red cell aggregation on attachment of neutrophils or platelets, which also assist their separate recruitment in venules or arteries. However, it has become increasingly evident that inflammatory and thrombotic responses may occur together, with platelets promoting the adhesion and activation of neutrophils and monocytes. Indeed, it is 30 years since we demonstrated that platelets could cause neutrophils to aggregate in suspension and, when attached to a surface, could support selectin-mediated rolling of all leukocytes. Thrombin-activated platelets could further induce neutrophil activation and immobilisation. In some conditions, platelets could bind to intact endothelial monolayers and capture neutrophils or monocytes. Subsequently, we found that extracellular vesicles released by activated platelets (PEV) fulfilled similar functions when deposited on surfaces or bound to endothelial cells. In murine models, platelets or PEV could act as bridges for monocytes in inflamed vessels. Thus, leukocytes and platelets are rheologically adapted for their separate functions, while novel thrombo-inflammatory pathways using platelets or PEV may underlie pathogenic leukocyte recruitment.

中文翻译：

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血栓炎症中白细胞、血小板和血管壁之间相互作用的流变学

白细胞和血小板必须粘附在血管壁上才能发挥其在炎症和止血中的保护功能。募集很大程度上取决于流变变量（壁剪切率和应力、红细胞聚集和血细胞比容），这些变量影响向血管壁的输送以及在那里经历的速度和力。白细胞募集仅在约 300 s−1 的壁剪切率下有效，并且通常仅限于炎症中的低剪切毛细血管后微静脉。由于较小，血小板在壁附近经历较低的速度和剪切力，并且可以以高得多的剪切速率粘附以实现动脉止血。此外，我们发现血细胞比容或红细胞聚集的变化对中性粒细胞或血小板附着的影响截然不同，这也有助于它们在小静脉或动脉中的单独募集。然而，越来越明显的是，炎症和血栓反应可能同时发生，血小板促进中性粒细胞和单核细胞的粘附和活化。事实上，我们已经证明血小板可以导致中性粒细胞在悬浮液中聚集，并且当附着在表面上时可以支持选择素介导的所有白细胞的滚动，这已经是 30 年前的事了。凝血酶激活的血小板可以进一步诱导中性粒细胞激活和固定。在某些情况下，血小板可以与完整的内皮单层结合并捕获中性粒细胞或单核细胞。随后，我们发现活化血小板（PEV）释放的细胞外囊泡在沉积在表面或与内皮细胞结合时发挥类似的功能。在小鼠模型中，血小板或 PEV 可以充当发炎血管中单核细胞的桥梁。因此，白细胞和血小板在流变学上适应了它们各自的功能，而使用血小板或PEV的新型血栓炎症途径可能是致病性白细胞募集的基础。