Cellular mechanisms in sepsis.
Cellular mechanisms in sepsis.
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DOI：
10.1177/0885066606297123
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发表时间：
2007-03-01
影响因子：
3.1
通讯作者：
Jean-Baptiste, Eddy
中科院分区：
文献类型：
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作者：
Jean-Baptiste, Eddy
尽管在重症监护室进行了先进的治疗，但脓毒症患者的死亡率仍然很高。脓毒性休克的发生是多因素的。组织损伤和器官功能障碍可能不仅是由微生物引起的，还可能是由对感染反应释放的炎症介质引起的。细胞因子（肿瘤坏死因子、白细胞介素-1、白细胞介素-6、白细胞介素-8、高迁移率组盒-1蛋白、巨噬细胞迁移抑制因子）和非细胞因子（一氧化氮、血小板活化因子、补体和类二十小体）可能造成组织损伤，并导致多器官功能障碍和细胞死亡（或凋亡）。革兰氏阴性菌是脓毒症患者中最常见的微生物。革兰氏阴性菌的病理作用是通过细菌细胞膜产生的脂多糖来传递的。脂多糖激活核因子κ B，从而触发炎症介质的释放。来自革兰氏阳性细菌、真菌或病毒的蛋白质成分可能以与脂多糖类似的方式激活核因子κ B。内源性抗炎介质在感染反应中释放，并起到控制压倒性全身炎症反应的作用。炎症介质负反馈和正反馈之间的脆弱平衡是调节细胞损伤和影响临床结果的关键因素。
Mortality remains very high among septic patients despite the advanced treatments rendered in intensive care units. The development of septic shock is multifactorial. Tissue damage and organ dysfunction may be caused not only by the microorganisms but also by the inflammatory mediators released in response to the infection. Cytokines (tumor necrosis factor, interleukin-1, interleukin-6, interleukin-8, high-mobility group box-1 protein, macrophage migratory inhibitory factor) and noncytokines (nitric oxide, platelet-activating factor, complements, and eicosonoids) may inflict tissue injury and contribute to multiple organ dysfunction and cell death (or apoptosis). Gram-negative bacteria are the most common organisms identified in septic patients. The pathological effects of gram-negative bacteria are conveyed through lipopolysaccharide derived from the bacterial cell membrane. Lipopolysaccharide activates the nuclear factor kappa B, which triggers the release of inflammatory mediators. Protein components from gram-positive bacteria, fungi, or viruses may evoke the activation of nuclear factor kappa B in a similar fashion as lipopolysaccharide. Endogenous anti-inflammatory mediators are released in response to the infection and act to control the overwhelming systemic inflammatory response. The fragile balance between negative and positive feedback on the inflammatory mediators is the key factor that modulates the cellular damage and influences the clinical outcome.