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J. Bacteriol. doi:10.1128/JB.01149-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The Response of Staphylococcus aureus to Salicylate Challenge

James T. Riordan, Arunachalam Muthaiyan, Wayne Van Voorhies, Christopher T. Price, James E. Graham, Brian J. Wilkinson, and John E. Gustafson*

Microbiology Group, Department of Biology, and Molecular Biology Program, New Mexico State University, Las Cruces, New Mexico 88003-8001, Department of Biological Sciences, Illinois State University, Normal, Illinois 61791-4120, and Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky, 40292

* To whom correspondence should be addressed. Email: jgustafs{at}nmsu.edu.


  Abstract

Growth of Staphylococcus aureus with the non-steroidal antiinflammatory salicylate reduces susceptibility of this organism to multiple antimicrobials. Transcriptome analysis reveals that growth of S. aureus with salicylate leads to the induction of genes involved with gluconate and formate metabolism, and represses genes required for gluconeogenesis and glycolysis. In addition, salicylate induction upregulates two antibiotic target genes and downregulates a multidrug efflux pump gene repressor (mgrA), and sarR, which represses a gene (sarA) important for intrinsic antimicrobial resistance. We hypothesize that these salicylate-induced alterations jointly represent a unique mechanism that allows S. aureus to resist antimicrobial stress and toxicity.




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