Abstract
Aspirin has been shown to cause a reduction in the virulence of Staphylococcus aureus–associated endocarditis. A new study reveals that salicylic acid, the major metabolite of aspirin, acts at the level of transcription to downregulate the production of fibrinogen, fibronectin, and α-hemolysin — virulence factors necessary for bacterial replication in host tissues and, now, potential therapeutic targets.
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