Salicylic acid: an old dog, new tricks, and staphylococcal disease
J. Clin. Invest. Mathias Herrmann, et al. 112:149 doi:10.1172/JCI19143 [
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Figure 2Potential roles of salicylic acid (SAL) in the pathogenesis of
S. aureus endovascular infection. (I) SAL pretreatment of
S. aureus results in overexpression of SigB-dependent genes in both an
rsbU-positive and an
rsbU-negative background, suggesting SigB activation independent of the anti–ς-factor RsbU. (II) Activation of the
sarAP3 promotor appears to contribute to decreased expression of active SarA protein, putatively via inhibitory activity of the
sarAP3 gene product. Again, SAL appears to contribute to SarA reduction in a
sarAP3-additive fashion. (III) As SarA controls expression of RNAII and RNAIII, the net effect of SAL is a mitigation of the
agr response. Since α-toxin (
hla) expression depends on both
sar and
agr, and expression of wall-bound adhesins is also in part controlled by
sar, the mitigation of both adhesin and toxin expression in SAL-treated microorganisms appears to depend on a combined
sar/
agr effect; yet other regulators may also be involved. (IV) In addition to
hla, the expression of other secreted molecules such as the extracellular adhesive protein Eap depends on
agr and
sarA and may be downregulated under the influence of SAL. Expression of the polysaccharide intracellular adhesin (PIA) is suggested to depend on
sigB, which may positively control expression of
icaADBC, with consequences not yet fully understood in
S. aureus endovascular infection. The
S. aureus adhesins (FnBPA, FnBPB, ClfA, and ClfB) recognize fibronectin and fibrinogen, which are presented on ECs and platelets.
