Neutrophil apoptosis in infectious disease
Neutrophil apoptosis in infectious disease
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DOI：
10.1080/01902140701756620
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发表时间：
2007-12-01
影响因子：
1.7
通讯作者：
Whyte, Moira K. B.
中科院分区：
文献类型：
--
作者：
Anwar, Sadia;Whyte, Moira K. B.
细胞凋亡或程序性细胞死亡是一种高度保守的细胞自杀机制。细胞凋亡对于炎症的有效解决至关重要，特别是在调节炎性中性粒细胞的寿命方面。中性粒细胞凋亡的病理性失调会阻止炎症的消退，并与许多炎症性疾病有关。同样，病原体对这种关键的宿主防御机制的破坏可以阻止感染的解决。下面，我们描述了不同细菌病原体对中性粒细胞凋亡调节的影响，并考虑如何重新参与这些被破坏的机制，可能有助于制定新的战略，以打击传染病。
Apoptosis, or programmed cell death, is a highly conserved cellular suicide mechanism. Apoptosis is critical to the effective resolution of inflammation, particularly in regulating the lifespan of the inflammatory neutrophil. Pathological dysregulation of neutrophil apoptosis prevents resolution of inflammation and is implicated in numerous inflammatory conditions. Similarly, subversion of this critical, host defense mechanism by pathogens can prevent resolution of infection. Below, we describe the effects of different bacterial pathogens on regulation of neutrophil apoptosis and consider how re-engagement of these subverted mechanisms may facilitate the develophtent of new strategies to combat infectious diseases.