Blériot Camille, Lecuit Marc
Institut Pasteur, Biology of Infection Unit, 75015, Paris, France.
U1117, Inserm, 75015, Paris, France.
Cell Mol Life Sci. 2016 Jun;73(11-12):2369-78. doi: 10.1007/s00018-016-2206-1. Epub 2016 Apr 5.
Necrosis has long been considered as a passive event resulting from a cell extrinsic stimulus, such as pathogen infection. Recent advances have refined this view and it is now well established that necrosis is tightly regulated at the cell level. Regulated necrosis can occur in the context of host-pathogen interactions, and can either participate in the control of infection or favor it. Here, we review the two main pathways implicated so far in bacteria-associated regulated necrosis: caspase 1-dependent pyroptosis and RIPK1/RIPK3-dependent necroptosis. We present how these pathways are modulated in the context of infection by a series of model bacterial pathogens.
长期以来，坏死一直被视为由细胞外源性刺激（如病原体感染）导致的被动事件。最近的进展完善了这一观点，现在已经明确坏死在细胞水平上受到严格调控。程序性坏死可发生在宿主与病原体相互作用的背景下，既可以参与感染控制，也可能促进感染。在此，我们综述了迄今为止与细菌相关的程序性坏死所涉及的两条主要途径：半胱天冬酶1依赖性细胞焦亡和受体相互作用蛋白激酶1/受体相互作用蛋白激酶3依赖性坏死性凋亡。我们展示了这些途径在一系列模式细菌病原体感染的背景下是如何被调节的。
