Unit Cytokines and Inflammation, Institut Pasteur, 28 rue Dr. Roux, 75015 Paris, France.
Curr Infect Dis Rep. 2007 Sep;9(5):358-65. doi: 10.1007/s11908-007-0056-6.
During sepsis, the plasma levels of numerous inflammatory markers are enhanced. Some of these markers are the mediators responsible for the syndromes observed during sepsis as well as for organ dysfunction and eventually death. Their role has been demonstrated in experimental models that employed either transgenic and gene-targeted animals or the use of neutralizing agents. Accordingly, anaphylatoxins generated after complement system activation, factors of coagulation and fibrinolysis, proinflammatory cytokines, chemokines, proteases, lipid mediators, nitric oxide, and cell markers of stress (eg, high mobility group box-1) have been shown to contribute to the deleterious events observed during sepsis. On the other hand, the counter-regulation of the inflammatory process, which involves mediators such as anti-inflammatory cytokines and some neuromediators, can jeopardize the immune status of the host and render the patients more sensitive to nosocomial infections.
在脓毒症中，大量炎症标志物的血浆水平升高。其中一些标志物是导致脓毒症期间观察到的综合征以及器官功能障碍并最终导致死亡的介质。它们的作用已在实验模型中得到证实，这些模型使用了转基因和基因靶向动物或使用了中和剂。因此，补体系统激活后产生的过敏毒素、凝血和纤溶因子、促炎细胞因子、趋化因子、蛋白酶、脂质介质、一氧化氮和应激细胞标志物（例如，高迁移率族蛋白框-1）已被证明有助于导致脓毒症期间观察到的有害事件。另一方面，炎症过程的反向调节涉及到抗炎细胞因子和一些神经递质等介质，可能危及宿主的免疫状态，并使患者更容易发生医院感染。
