Staphylococcus aureus Exploits a Non-ribosomal Cyclic Dipeptide to Modulate Survival within Epithelial Cells and Phagocytes
Fig 2
Synthetic phevalin increases phagosomal escape rates of S. aureus.
a) At the time of infection, 10 μM phevalin was added simultaneous with S. aureus JE2 wild type (WT) or mutant strains to host cells. Concentration-dependent increase in phagosomal escape rates of bacteria was observed in the phevalin-treated samples when compared to solvent control. b) Phevalin does not act as calpain inhibitor. During infection with S. aureus (WT), host cells were either treated with 10 μM phevalin (Phe), calpain inhibitor I (Calp I), Calpeptin, or solvent control (DMSO). Whereas Calp I and Calpeptin caused a significant reduction of S. aureus phagosomal escape, phevalin did not, thereby suggesting a different mode of action of the pyrazinone. Bar graphs show the mean of three independent experiments ± SD. Statistical analysis was performed by t-test. *P<0.05; **P<0.01; ***P<0.001.