Although, it is still unclear if the increased transcription of these virulence determinants lead to increased amounts of SE proteins. Furthermore, identification of the environmental parameters that control the expression of SEA in food, and the mechanism by which these signals are transduced to bring about changes in gene expression, are very limited. This knowledge is Saracatinib datasheet FGFR inhibitor crucial for understanding the potential of S. aureus to cause food poisoning. Acetic acid is a weak

organic acid often used in the food industry as a preservative due to its antagonistic effect on bacterial pathogens [15]. Weak acids have the ability to pass through the cell membrane in the undissociated form. Once inside the cell, the acid dissociates in the more alkaline interior, lowering the intracellular pH of the cell. A decrease in intracellular pH can lead to the damage of macromolecules (e.g. proteins and DNA) and the cell membrane, and have a negative

effect on cell maintenance [16, 17]. Also, the anion of the acid is accumulated intracellularly, increasing turgor pressure [18]. Acetic acid has been found to be more inhibitory to the growth of S. aureus than lactic acid, citric acid, phosphoric acid and hydrochloric acid, respectively [19]. Also, acetic find more acid has been found to almost completely inhibit SEA formation in brain heart infusion (BHI) broth when added gradually over time [20]. In the present study, the effects

of acetic acid on S. aureus growth, sea expression and SEA production were investigated in four growth phases. Furthermore, the relationship between SEA production Mannose-binding protein-associated serine protease and the lifecycle of the phage carrying the toxin gene was determined. Finally, genomic analysis of S. aureus strains carrying sea was performed to map differences within the gene and in the temperate phage carrying sea. Results Effects of acetic acid on sea expression and SEA production in S. aureus Mu50 Batch cultures of S. aureus Mu50, harboring the sea-containing Φ42-like prophage ΦMu50A [21], were carried out at controlled pH levels of 7.0, 6.5, 6.0, 5.5, 5.0, and 4.5 (Figure 1A). Acetic acid was used to set the pH to investigate the effects of acetic acid on growth, relative sea expression and extracellular SEA levels during all stages of growth. The maximal growth rate of S. aureus Mu50 was highest at pH 7.0 and decreased with decreasing pH (Figure 1A). Batch cultivations performed at lower pH values showed that pH 5.0 was highly growth-inhibitory, with only a modest increase in optical density, OD, and viable cells in the late stationary growth phase, and that pH 4.5 was too toxic; < 1% of the starting inoculum was viable after 24 h.