This Article Full Text Full Text (PDF) Other Versions of this Article: JB.01149-06v1 189/1/220    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Riordan, J. T. Articles by Gustafson, J. E. Search for Related Content PubMed PubMed Citation Articles by Riordan, J. T. Articles by Gustafson, J. E.

Response of Staphylococcus aureus to Salicylate Challenge

Microbiology Group, Department of Biology,¹ Molecular Biology Program, New Mexico State University, Las Cruces, New Mexico 88003-8001,² Department of Biological Sciences, Illinois State University, Normal, Illinois 61791-4120,³ Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky 40292⁴

Received 23 July 2006/ Accepted 10 October 2006

Growth of Staphylococcus aureus with the nonsteroidal anti-inflammatory salicylate reduces susceptibility of the organism to multiple antimicrobials. Transcriptome analysis revealed 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.

Published ahead of print on 20 October 2006.