先天免疫与凝血。
Innate immunity and coagulation.
机构信息
Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
出版信息
J Thromb Haemost. 2011 Jul;9 Suppl 1(Suppl 1):182-8. doi: 10.1111/j.1538-7836.2011.04323.x.
Abstract
Infection frequently elicits a coagulation response. Endotoxin triggers the formation of tissue factor initiating coagulation, down regulates anticoagulant mechanisms including the protein C pathway and heparin-like proteoglycans and up regulates plasminogen activator inhibitor. The overall physiological result of this is to promote coagulation through enhancing initiation, suppressing negative regulation and impairing fibrin removal. The response to infection also leads to tissue destruction. Nucleosomes and histones released from the injured cells trigger further inflammation, protection from the pathogen but further tissue injury leading to multi-organ failure. Such a complex response to infection presumably arises due to the role of coagulation in the control and clearance of the infectious agent.
摘要
感染通常会引发凝血反应。内毒素触发组织因子的形成，启动凝血，下调抗凝机制，包括蛋白 C 途径和肝素样糖蛋白，并上调纤溶酶原激活物抑制剂。其整体生理结果是通过增强启动、抑制负调节和损害纤维蛋白溶解来促进凝血。对感染的反应也会导致组织破坏。受损细胞释放的核小体和组蛋白进一步引发炎症，起到抵御病原体的作用，但也会导致进一步的组织损伤，从而导致多器官衰竭。这种对感染的复杂反应可能是由于凝血在控制和清除感染因子中的作用所致。
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