Skip to main content
. Author manuscript; available in PMC: 2008 Dec 10.
Published in final edited form as: Curr Immunol Rev. 2006 May;2(2):119–141. doi: 10.2174/157339506776843033

Fig. (2).

Fig. (2)

Programmed cell death (PCD) regulatory activities of gram-positive bacterial apoptosis regulatory molecules (ARMs). Numerous bacterial ARMs commandeer different elements of the intrinsic and extrinsic PCD pathways to seize control of the apoptotic machinery of the host cell; an activity that may improve the microbe’s survival and persistence. In S. aureus infection (A), α-toxin causes pores to form in the host cell membrane, which disrupts ionic balance, and alters steady state intrinsic mitochondrial PCD activity. Additionally, SEB triggers activation-induced cell death in T cells by a mechanism centered on extrinsic PCD factors involving FAS-FASL signaling. LeTx produced by B. anthracis (B) inhibits MAPK activity in macrophages and triggers PCD by a mechanism that involves activation of caspase-8. PCD in activated T cells in response to L. monocytogenes listeriolysin O (C) is characterized by a variety of alterations in both the intrinsic and extrinsic PCD pathways. Perforin and IFN-γ appear to contribute to these alterations. Finally, PCD in intestinal enterocytes triggered by C. difficile exotoxin (D) is executed by inactivation of Rho GTPases and involves toxin-induced alterations in both the intrinsic and extrinsic PCD pathways.