Yao Yong-Ming, Luan Ying-Yi, Zhang Qing-Hong, Sheng Zhi-Yong
Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, 51 Fu-cheng Road, Haidian District, Beijing, 100048, People's Republic of China.
Methods Mol Biol. 2015;1237:5-15. doi: 10.1007/978-1-4939-1776-1_2.
Sepsis is defined as severe systemic inflammation in response to invading pathogens, or an uncontrolled hyperinflammatory response, as mediated by the release of various proinflammatory mediators. Although some patients may die rapidly from septic shock accompanied by an overwhelming systemic inflammatory response syndrome (SIRS) triggered by a highly virulent pathogen, most patients survive the initial phase of sepsis, showing multiple organ damage days or weeks later. These patients often demonstrate signs of immune suppression accompanied by enhanced inflammation. Sepsis is a result of a complex process; there is interaction of various pathways, such as inflammation, immunity, coagulation, as well as the neuroendocrine system. This treatise is an attempt to provide a summary of several key regulatory mechanisms and to present the currently recognized molecular pathways that are involved in the pathogenesis of sepsis.
脓毒症被定义为机体对入侵病原体作出的严重全身炎症反应，或由多种促炎介质释放介导的失控性过度炎症反应。尽管一些患者可能因高毒力病原体引发的严重全身炎症反应综合征（SIRS）导致的感染性休克而迅速死亡，但大多数患者在脓毒症初始阶段存活下来，数天或数周后出现多器官损伤。这些患者常表现出免疫抑制迹象并伴有炎症增强。脓毒症是一个复杂过程的结果；存在多种途径的相互作用，如炎症、免疫、凝血以及神经内分泌系统。本论文旨在总结几种关键调节机制，并介绍目前公认的参与脓毒症发病机制的分子途径。
