Department of Internal Medicine and Cardiology, Center for Venous Thromboembolism Disease, Medical University of Warsaw, Warsaw, Poland.
Department of Internal and Agricultural Medicine, Jagiellonian University Medical College, Krakow, Poland.
Arch Immunol Ther Exp (Warsz). 2024 Jan 24;72(1). doi: 10.2478/aite-2024-0003. eCollection 2024 Jan 1.
Venous thromboembolism, encompassing acute pulmonary embolism (APE) and deep vein thrombosis (DVT), is a potentially fatal disease with complex pathophysiology. Traditionally, the Virchow triad provided a framework for understanding the pathogenic contributors to thrombus formation, which include endothelial dysfunction, alterations in blood flow and blood hypercoagulability. In the last years, it has become apparent that immunity plays a central role in thrombosis, interacting with classical prothrombotic mechanisms, oxidative stress and vascular factors. Thrombosis amplifies inflammation, and exaggerated inflammatory processes can trigger thrombosis mainly due to the activation of leukocytes, platelets, and endothelial cells. APE-related endothelium injury is a major trigger for immune system activation. Endothelium is also a key component mediating inflammatory reaction and it is relevant to maintain vascular permeability. Exaggerated right ventricular wall stress and overload, with coexisting systemic hypotension and hypoxemia, result in myocardial injury and necrosis. Hypoxia, tissue factor activation and cytokine storm are engaged in the thrombo-inflammatory processes. Thrombus development is characterized by inflammatory state vascular wall caused mainly by an early extravasation of leukocytes and intense selectins and cytokines production. Nevertheless, immunity of DVT is well described, little is known about potential chemokine and cellular differences between thrombus that develops in the vein and thrombus that detaches and lodges in the pulmonary circulation being a cause of APE. There is a paucity of data considering inflammatory state in the pulmonary artery wall during an acute episode of pulmonary embolism. The main aim of this review is to summarize the knowledge of immunity in acute phase of pulmonary embolism in experimental models.
静脉血栓栓塞症，包括急性肺栓塞（APE）和深静脉血栓形成（DVT），是一种具有复杂病理生理学的潜在致命疾病。传统上，Virchow 三联征为理解血栓形成的致病因素提供了一个框架，这些因素包括内皮功能障碍、血流改变和血液高凝状态。在过去的几年中，人们已经清楚地认识到，免疫在血栓形成中起着核心作用，与经典的促血栓形成机制、氧化应激和血管因素相互作用。血栓形成会放大炎症，而过度的炎症过程会主要由于白细胞、血小板和内皮细胞的激活而引发血栓形成。APE 相关的内皮损伤是免疫系统激活的主要触发因素。内皮也是介导炎症反应的关键组成部分，与维持血管通透性有关。右心室壁应力和负荷过度，同时伴有系统性低血压和低氧血症，导致心肌损伤和坏死。缺氧、组织因子激活和细胞因子风暴参与血栓炎症过程。血栓形成的特征是炎症状态的血管壁，主要由白细胞早期渗出和强烈的选择素和细胞因子产生引起。然而，DVT 的免疫机制已得到很好的描述，对于在静脉中形成的血栓和在肺循环中脱落和滞留的血栓之间的潜在趋化因子和细胞差异知之甚少，后者是 APE 的一个原因。在急性肺栓塞发作期间，肺动脉壁炎症状态的数据很少。本综述的主要目的是总结实验模型中急性肺栓塞阶段免疫的相关知识。
