Perfringolysin O-Induced Plasma Membrane Pores Trigger Actomyosin Remodeling and Endoplasmic Reticulum Redistribution

摘要: Clostridium perfringens produces an arsenal of toxins that act together to cause severe infections in humans and livestock animals. Perfringolysin O (PFO) is a cholesterol-dependent pore-forming toxin encoded the chromosome virtually all C. strains acts synergy with other determine outcome infection. However, its individual contribution disease poorly understood. Here, we intoxicated human epithelial endothelial cells purified PFO evaluate host cytoskeletal responses PFO-induced damage. We found that, at sub-lytic concentrations, induces profound reorganization actomyosin cytoskeleton culminating into assembly well-defined cortical structures sites plasma membrane (PM) remodeling. The such occurs concomitantly loss PM integrity requires pore-formation, calcium influx, myosin II activity. recovery from damage simultaneously disassembly structures. also targets endoplasmic reticulum (ER) by inducing disruption vacuolation. ER-enriched vacuoles were detected cell cortex within These cellular events suggest targeting endothelium early stages infection, which secreted concentrations.