The pathogenesis of sepsis.

The pathogenesis of sepsis.
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DOI:
10.1146/annurev-pathol-011110-130327
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发表时间:
2011
期刊:
Annual review of pathology
影响因子:
--
通讯作者:
Remick DG
Remick DG
中科院分区:
其他
文献类型:
--
作者:
Stearns-Kurosawa DJ;Osuchowski MF;Valentine C;Kurosawa S;Remick DG

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脓毒症是一种严重的临床疾病,代表患者对严重感染的反应,死亡率很高。正常的免疫和生理反应可以根除病原体,而脓毒症的病理生理是由于这些正常反应的不适当调节。在理想的情况下,病原体与炎症系统的第一次接触应该消除微生物,并迅速使宿主恢复体内平衡。由于中性粒细胞和巨噬细胞/单核细胞的持续活化,脓毒性反应可能会加速。淋巴细胞共刺激分子的上调和淋巴细胞的快速凋亡、中性粒细胞的延迟凋亡以及细胞/组织坏死的增强也是脓毒症的发病机制之一。凝血系统与炎症反应密切相关,两个系统之间的串扰驱动了失调的反应。生物标记物可用于帮助诊断脓毒症患者,也可用于识别从免疫调节疗法中获益的患者。
Sepsis is a serious clinical condition that represents a patient’s response to a severe infection and has a very high mortality rate. Normal immune and physiologic responses eradicate pathogens, and the pathophysiology of sepsis is due to the inappropriate regulation of these normal reactions. In an ideal scenario, the first pathogen contact with the inflammatory system should eliminate the microbe and quickly return the host to homeostasis. The septic response may accelerate due to continued activation of neutrophils and macrophages/monocytes. Upregulation of lymphocyte costimulatory molecules and rapid lymphocyte apoptosis, delayed apoptosis of neutrophils, and enhanced necrosis of cells/tissues also contribute to the pathogenesis of sepsis. The coagulation system is closely tied to the inflammatory response, with cross talk between the two systems driving the dysregulated response. Biomarkers may be used to help diagnose patients with sepsis, and they may also help to identify patients who would benefit from immunomodulatory therapies.
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