Altered toxicity of Staphylococcus aureus and its membrane vesicles following ethanol and glycidol exposure

Since Staphylococcus aureus is subjected to a variety of environmental stresses, including chemicals, when encountering the host during infection, this study investigated the effects of ethanol and glycidol on virulent phenotype of S. aureus and its membrane vesicles (MVs). Ethanol increased staphylococcal enterotoxin A (SEA) production approximately twofold at all concentrations tested, while glycidol induced a fivefold increase above 100 mM. Both agents upregulated the expression of sak , a phage-encoded gene akin to SEA; cro , a lysis-related gene, and recA , linked to the SOS response and DNA repair. Ethanol (1.0%) and glycidol (100 mM) also increased the expression of RNAIII, icaA (biofilm formation), and hlb (β-hemolytic toxin), resulting in increased biofilm formation. Ethanol and glycidol augmented S. aureus virulence and influenced MV properties. Ethanol boosted hemolytic toxin activity in culture supernatants and MVs, whereas glycidol reduced it in MVs without affecting supernatants. While ethanol did not alter SEA content in MVs, glycidol increased it, along with the internalization of specific cargo proteins. Additionally, glycidol-derived MVs enhanced IFN-γ expression in mouse spleen cells. These findings suggest that ethanol and glycidol exposure may drive S. aureus toward a more virulent phenotype, accompanied by increased MV toxicity. • Ethanol and glycidol increased staphylococcal enterotoxin A (SEA) production • Ethanol and glycidol enhanced S. aureus virulence factor expression • Ethanol and glycidol enhanced biofilm formation • Glycidol increased the amount of SEA in S. aureus membrane vesicles (MVs) • Glycidol enhanced internalization of several cargo proteins in S. aureus MVs • MVs from glycidol-treated S. aureus increased IFN-γ expression in mouse spleen cells