Cytokines as mediators in the pathogenesis of septic shock.
Cytokines as mediators in the pathogenesis of septic shock.
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DOI：
10.1007/978-3-642-80186-0_7
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发表时间：
1996
影响因子：
--
通讯作者：
C. A. Dinarello
中科院分区：
文献类型：
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作者：
C. A. Dinarello
在感染性休克期间，宿主产生几种促炎细胞因子，这些细胞因子在疾病的发病机制中起着关键作用。这些细胞因子的产生是由生物体自身（吞噬作用）或生物体的可溶性产物引起的。例如，革兰氏阴性菌的脂多糖内毒素（LPS），革兰氏阳性菌的蛋白质外毒素，以及细胞壁糖肽类物质，如磷壁酸和muramyl肽。当然，到目前为止，脂多糖是细菌诱导细胞因子产生的最有效的可溶性产物，因此大多数关于细胞因子诱导的信息来自体外和体内使用脂多糖的研究。然而，重要的是要认识到，在感染性休克中细胞因子的产生既不特定也不独特。导致感染性休克病理改变的细胞因子并不是感染所特有的。多重创伤、缺血再灌注损伤、急性移植排斥反应、抗原特异性免疫反应和各种急性炎症状态（急性肝炎和胰腺炎）启动相同的细胞因子级联并导致全身和局部炎症过程。
During septic shock the host produces several proinflammatory cytokines which have been implicated as playing a critical role in the pathogenesis of the disease. The production of these cytokines is initiated by the organisms themselves (phagocytosis) or by soluble products of the organisms. For example, the lipopolysaccharide endotoxins (LPS) of gram-negative bacteria, the protein exotoxins of gram-positive bacteria, and the cell-wall glycopeptides such as teichoic acids and muramyl peptides. Of course, LPS is by far the most potent soluble product of bacteria which induces cytokine production, and therefore most information about cytokine induction is derived from studies using LPS in vitro and in vivo. However, it is important to recognize that the cytokine production in septic shock is neither specific nor unique. The cytokines which contribute to pathological changes in septic shock are not unique to infection. Multiple trauma, ischemia-reperfusion injury, acute transplant rejection, antigen-specific immune responses, and various acute inflammatory states (acute hepatitis and pancreatitis) initiate the same cytokine cascade and result in both systemic and local inflammatory processes.