Department of Biochemistry, Institute of Biology, State University of Campinas.
Braz J Infect Dis. 2009 Jun;13(3):226-31. doi: 10.1590/s1413-86702009000300014.
Several pathogenic or opportunistic bacteria have the ability to either induce or inhibit host cell apoptosis. The capacity to modulate cell pathways that result in the induction or delay of host cell apoptosis is considered to be an important bacterial virulence mechanism. These processes could be mediated by different host cell signaling pathways that are subverted by the bacteria. Pathogens are able to activate apoptotic proteins, such as caspases, or inactivate anti-apoptotic proteins, such as NFkB and the MAPKKs, or even up-regulate the endogenous receptor/ligand system that induces apoptosis, generally when the bacteria are bound to the host cell surface. The bacteria-induced apoptotic or anti-apoptotic processes are often related with the fact that the bacteria acquire the ability to reach the host tissues. However, apoptosis is also considered to be a host defense mechanism against infectious agents. Thus, the apoptosis phenomenon plays a central role in host-pathogen interactions.
几种病原或机会性病原体具有诱导或抑制宿主细胞凋亡的能力。调节导致宿主细胞凋亡诱导或延迟的细胞途径的能力被认为是一种重要的细菌毒力机制。这些过程可以通过不同的宿主细胞信号通路来介导,这些信号通路被细菌颠覆。病原体能够激活凋亡蛋白,如半胱天冬酶,或失活抗凋亡蛋白,如 NFkB 和 MAPKKs,甚至上调诱导凋亡的内源性受体/配体系统,通常当细菌与宿主细胞表面结合时。细菌诱导的凋亡或抗凋亡过程通常与细菌获得到达宿主组织的能力有关。然而,凋亡也被认为是宿主对抗感染因子的防御机制。因此,凋亡现象在宿主-病原体相互作用中起着核心作用。