Luan Ying-yi, Yao Yong-ming, Xiao Xian-zhong, Sheng Zhi-yong
1 Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital , Beijing, People's Republic of China .
J Interferon Cytokine Res. 2015 Jan;35(1):17-22. doi: 10.1089/jir.2014.0069. Epub 2014 Jul 9.
Sepsis with subsequent multiple-organ dysfunction is a distinct systemic inflammatory response to concealed or obvious infection, and it is a leading cause of death in intensive care units. Thus, one of the key goals in critical care medicine is to develop novel therapeutic strategies that will affect favorably on outcome of septic patients. In addition to systemic response to infection, apoptosis is implicated to be an important mechanism of the death of immune cells, including neutrophils, macrophages, T lymphocytes, and dendritic cells, and it is usually followed by the development of multiple-organ failure in sepsis. The implication of apoptosis of immune cells is now highlighted by multiple studies that demonstrate that prevention of cell apoptosis can improve survival in relevant animal models of severe sepsis. In this review, we focus on major apoptotic death pathways and molecular mechanisms that regulate apoptosis of different immune cells, and advances in these areas that may be translated into more promising therapies for the prevention and treatment of severe sepsis.
伴有随后多器官功能障碍的脓毒症是对隐匿性或显性感染的一种独特的全身炎症反应,并且是重症监护病房中死亡的主要原因。因此,重症医学的关键目标之一是开发能对脓毒症患者的预后产生有利影响的新型治疗策略。除了对感染的全身反应外,细胞凋亡被认为是免疫细胞死亡的重要机制,包括中性粒细胞、巨噬细胞、T淋巴细胞和树突状细胞,并且在脓毒症中通常随后会发生多器官衰竭。多项研究突出了免疫细胞凋亡的影响,这些研究表明预防细胞凋亡可提高严重脓毒症相关动物模型的存活率。在本综述中,我们聚焦于调节不同免疫细胞凋亡的主要凋亡死亡途径和分子机制,以及这些领域的进展,这些进展可能转化为预防和治疗严重脓毒症更有前景的疗法。