Marsh C B, Wewers M D
Department of Internal Medicine, Ohio State University College of Medicine, Columbus, USA.
Clin Chest Med. 1996 Jun;17(2):183-97. doi: 10.1016/s0272-5231(05)70308-7.
Gram-negative bacteria gain access to the bloodstream by evading host defenses. Once in circulation, lipopolysaccharide interacts with the host receptor CD14 and initiates the host's immune response. Lipolysaccharide stimulates the host to produce a cascade of mediators that activate and target leukocytes, opsonize the bacteria, and induce fever to defend against the invading bacteria. Unregulated release of these mediators, however, leads to the production of vasoactive substances, activation of the clotting cascade, and diminution of cardiac performance, which leads to the sepsis syndrome. This article discusses the pathogenic events that lead to sepsis syndrome and reviews critical steps in regulating these inflammatory mediators to allow the host to recover from gram-negative bacteremia.
革兰氏阴性菌通过逃避宿主防御进入血液循环。一旦进入循环系统，脂多糖就会与宿主受体CD14相互作用并启动宿主的免疫反应。脂多糖刺激宿主产生一系列介质，这些介质可激活并靶向白细胞、调理细菌以及引发发热以抵御入侵的细菌。然而，这些介质的不受控制释放会导致血管活性物质的产生、凝血级联反应的激活以及心脏功能的减弱，进而导致脓毒症综合征。本文讨论了导致脓毒症综合征的致病过程，并回顾了调节这些炎症介质的关键步骤，以使宿主从革兰氏阴性菌血症中恢复。
