Abstract
Pore-forming bacterial toxins are considered to be the principal virulence factors contributing to severe inflammatory diseases in humans and animals. The pore-forming toxins are released from Gram-negative bacteria as soluble monomeric proteins, which then assemble into oligomeric pores on their target cell membranes. These toxins induce inflammation through their unique pore-forming ability and concomitant cytolysis of their host cells. However, the actions of these toxins are concentration-dependent, that is, high concentrations of toxins cause cytolysis, whereas sub-lytic concentrations of toxin cause a cellular activation that generates various proinflammatory mediators. Most studies have focused on the mechanisms of pore formation by these toxins, and little effort has been given to exploring the mechanisms underlying their induction of cellular activation cascades.
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