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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Inflammation, endothelium, and coagulation in sepsis.
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Inflammation, endothelium, and coagulation in sepsis.

机译：脓毒症中的炎症，内皮细胞和凝血。

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摘要

Sepsis is a systemic response to infection, and symptoms are produced by host defense systems rather than by the invading pathogens. Amongst the most prominent features of sepsis, contributing significantly to its outcome, is activation of coagulation with concurrent down-regulation of anticoagulant systems and fibrinolysis. Inflammation-induced coagulation on its turn contributes to inflammation. Another important feature of sepsis, associated with key symptoms such as hypovolemia and hypotension, is endothelial dysfunction. Under normal conditions, the endothelium provides for an anticoagulant surface, a property that is lost in sepsis. In this review, data about the interplay between inflammation and coagulation in sepsis are summarized with a special focus on the influence of the endothelium on inflammation-induced coagulation and vice versa. Possible procoagulant properties of the endothelium are described, such as expression of tissue factor (TF) and von Willebrand factor and interaction with platelets. Possible procoagulant roles of microparticles, circulating endothelial cells and endothelial apoptosis, are also discussed. Moreover, the important roles of the endothelium in down-regulating the anticoagulants TF pathway inhibitor, antithrombin, and the protein C (PC) system and inhibition of fibrinolysis are discussed. The influence of coagulation on its turn on inflammation and the endothelium is described with a special focus on protease-activated receptors (PARs). We conclude that the relationship between endothelium and coagulation in sepsis is tight and that further research is needed, for example, to better understand the role of activated PC signaling via PAR-1, the role of the endothelial PC receptor herein, and the role of the glycocalyx.
机译：败血症是对感染的系统性反应，症状是由宿主防御系统而非入侵的病原体产生的。脓毒症的最突出特征（对脓毒症的疗效有重要贡献）是凝血的激活，同时抗凝系统和纤维蛋白溶解的下调。炎症诱导的凝结反过来会导致炎症。败血症的另一个重要特征是与内皮功能障碍有关，而败血症与血容量不足和低血压等关键症状有关。在正常情况下，内皮提供抗凝表面，这是败血症丧失的特性。在这篇综述中，总结了脓毒症中炎症与凝血之间相互作用的数据，并特别关注了内皮对炎症诱导的凝血的影响，反之亦然。描述了内皮的可能的促凝特性，例如组织因子（TF）和血管性血友病因子的表达以及与血小板的相互作用。还讨论了微粒，循环内皮细胞和内皮细胞凋亡可能的促凝作用。此外，还讨论了内皮在下调抗凝剂TF途径抑制剂，抗凝血酶和蛋白C（PC）系统以及抑制纤维蛋白溶解中的重要作用。描述了凝血对其炎症和内皮的影响，特别关注蛋白酶激活受体（PARs）。我们得出结论，脓毒症中内皮细胞与凝血之间的关系紧密，需要进一步研究，例如，以更好地了解通过PAR-1激活的PC信号传导的作用，本文中内皮PC受体的作用以及糖萼。

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