CLOSTRIDIUM-PERFRINGENS ENTEROTOXIN ACTS BY PRODUCING SMALL-MOLECULE PERMEABILITY ALTERATIONS IN PLASMA-MEMBRANES

Clostridium perfringens enterotoxin (CPE) appears to utilize a unique mechanism of action to directly affect the plasma membrane permeability of mammalian cells. CPE action involves a multi-step action which culminates in cytotoxicity. Initially CPE binds to a protein receptor on mammalian plasma membranes. The membrane-bound CPE then becomes progressively more resistant to release by proteases (a phenomenon consistent with the insertion of CPE into membranes). This 'inserted' CPE then participates in the formation of a large complex in plasma membranes which contains one CPE: one 70 kDa membrane protein: one 50 kDa membrane protein. Upon formation of large complex, plasma membranes become freely permeable to small molecules such as ions and amino acids. This CPE-induced disruption of the cellular colloid-osmotic equilibrium then causes secondary cellular effects and cell death.