Salicylic acid attenuates virulence in endovascular infections by targeting global regulatory pathways in Staphylococcus aureus
J. Clin. Invest. Leon Iri Kupferwasser, et al. 112:222 doi:10.1172/JCI16876 [Go to this article.]

Figure 3
(a) Flow cytometric analysis of salicylic acid–induced effects on sar-gfp_uvr constructs. In S. aureus RN6390, flow cytometry demonstrated a 2.5-fold attenuation of P1-initiated sarA promoter activity (left) and a 1.8-fold increase of P3-initiated sarA promoter activity (right) in cultures pre-exposed to salicylic acid (50 μg/ml) as compared with expression in plain medium. (b) Effect of salicylic acid on sar promoter transcription in S. aureus. Northern analysis revealed that in S. aureus RN6390 cells precultured in the presence of 50 μg/ml salicylic acid, P1-initiated sarA transcription was suppressed, whereas P3-initiated sarA transcription (corresponds to sarC) was enhanced in the late log phase and postexponential phase, as compared with cells precultured in plain medium. The P2-initiated sarA transcription level (corresponds to sarB) was too weak to define the impact of salicylic acid on this locus.