α-Hemolysin (Staphylococcus aureus), a polypeptide virulence factor of Staphylococcus aureus, disrupts host cell plasma membranes. Upon binding to the cell surface, its monomers create a homoheptamic prepore, which evolves into a mature transmembrane pore, facilitating K+ and Ca2+ ion transport that induces necrotic death in target cells [1].

α-Hemolysin (Staphylococcus aureus) induces IL-1β secretion and caspase-1 activation in THP-1 cells via NLRP3 inflammasome-dependent caspase-1 activation [1]. Additionally, α-hemolysin (Staphylococcus aureus)(1 µg/mL, 4h) triggers cell death in derivatives of THP cells, which requires host NLRP3 signaling but is independent of caspase-1 activation and IL-1β secretion [1].