Procoagulant activities in human alveolar macrophages.

B Nakstad, N P Boye, T Lyberg
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Abstract

The coexistence of fibrin and tissue macrophages is a common finding in the histopathology of chronic lung inflammatory diseases. Human lung alveolar macrophages (LAM) obtained by lavage of healthy donors can initiate the coagulation sequence by expressing procoagulant factors. The procoagulants of LAM were in this study identified to be either thromboplastin (tissue factor) or a direct factor X activator, probably a thromboplastin/factor VII complex. LAM did not show inducible thromboplastin synthesis as did monocytes when stimulated in vitro. LAM were separated into four subpopulations by density gradient centrifugation. The specific thromboplastin activity of subpopulation cells varied inversely with their density. Low-density subpopulations of LAM released microvesicles from their surface which could be recovered in the culture medium, and which expressed procoagulant activities with the same characteristics as the LAM procoagulants. These findings suggest that alveolar macrophages and the membrane vesicles shed from their surface contribute to local fibrin deposition in the lungs by expressing procoagulant factors.

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人肺泡巨噬细胞的促凝活性。
纤维蛋白与组织巨噬细胞共存是慢性肺部炎症性疾病组织病理学的共同发现。人肺泡巨噬细胞(LAM)通过对健康供体进行灌洗获得,可通过表达促凝因子启动凝血序列。在本研究中,LAM的促凝剂被确定为凝血活素(组织因子)或直接因子X激活剂,可能是凝血活素/因子VII复合物。LAM在体外刺激时不像单核细胞那样表现出可诱导的凝血活素合成。采用密度梯度离心分离法将蓝莓分为4个亚群。亚群细胞的特异性凝血活素活性与密度成反比。低密度的LAM亚群从其表面释放出微囊泡,这些微囊泡可以在培养基中回收,并且表达与LAM促凝剂相同的促凝活性。这些发现表明,肺泡巨噬细胞及其表面脱落的膜泡通过表达促凝因子参与肺局部纤维蛋白沉积。
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