Sepsis accounts for nearly 700 000 deaths in Europe annually and is caused by an overwhelming host response to infection resulting in organ failure. The endothelium is an active contributor to sepsis and as such represents a major target for therapy. During sepsis, endothelial cells amplify the immune response and activate the coagulation system. They are both a target and source of inflammation and serve as a link between local and systemic immune responses. In response to cytokines produced by immune cells, the endothelium expresses adhesion molecules and produces vasoactive compounds, inflammatory cytokines, and chemoattractants, thus switching from an anticoagulant to procoagulant state. These responses contribute to local control of infection, but systemic activation can lead to microvascular thrombosis, capillary permeability, hypotension, tissue hypoxia, and ultimately tissue damage. This review focuses on the role of the endothelium in leucocyte adhesion and transmigration as well as production of reactive oxygen and nitrogen species, microRNAs and cytokines, formation of signalling microparticles, and disseminated intravascular coagulation. We also discuss alterations in endothelial permeability and apoptosis. Finally, we review the diagnostic potential of endothelial markers and endothelial pathways as therapeutic targets for this devastating disease.

中文翻译：

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脓毒症对内皮的影响和临床意义

脓毒症每年在欧洲造成近 70 万人死亡，它是由宿主对感染的强烈反应导致器官衰竭引起的。内皮是脓毒症的积极贡献者，因此是治疗的主要目标。在败血症期间，内皮细胞会放大免疫反应并激活凝血系统。它们既是炎症的靶点，也是炎症的源头，并作为局部和全身免疫反应之间的纽带。响应免疫细胞产生的细胞因子，内皮表达粘附分子并产生血管活性化合物、炎性细胞因子和化学引诱物，从而从抗凝剂状态转变为促凝剂状态。这些反应有助于局部控制感染，但全身激活可导致微血管血栓形成、毛细血管通透性、低血压、组织缺氧，最终造成组织损伤。本综述重点关注内皮在白细胞粘附和迁移中的作用，以及活性氧和氮的产生、微小 RNA 和细胞因子、信号微粒的形成和弥散性血管内凝血。我们还讨论了内皮通透性和细胞凋亡的改变。最后，我们回顾了内皮标志物和内皮通路作为这种破坏性疾病的治疗靶点的诊断潜力。我们还讨论了内皮通透性和细胞凋亡的改变。最后，我们回顾了内皮标志物和内皮通路作为这种破坏性疾病的治疗靶点的诊断潜力。我们还讨论了内皮通透性和细胞凋亡的改变。最后，我们回顾了内皮标志物和内皮通路作为这种破坏性疾病的治疗靶点的诊断潜力。