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Antimicrobial Agents and Chemotherapy, March 2005, p. 916-924, Vol. 49, No. 3
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.3.916-924.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Induction of Fibronectin Adhesins in Quinolone-Resistant Staphylococcus aureus by Subinhibitory Levels of Ciprofloxacin or by Sigma B Transcription Factor Activity Is Mediated by Two Separate Pathways

Dongmei Li,1,{dagger} Adriana Renzoni,1,{dagger} Tristan Estoppey,1 Carmelo Bisognano,1 Patrice Francois,1 William L. Kelley,1 Daniel P. Lew,1 Jacques Schrenzel,1 and Pierre Vaudaux1*

Service of Infectious Diseases, University Hospitals of Geneva, Geneva, Switzerland1

Received 30 June 2004/ Returned for modification 13 August 2004/ Accepted 8 November 2004

We recently reported on the involvement of a RecA-LexA-dependent pathway in the ciprofloxacin-triggered upregulation of fibronectin-binding proteins (FnBPs) by fluoroquinolone-resistant Staphylococcus aureus. The potential additional contribution of the transcription factor sigma B (SigB) to the ciprofloxacin-triggered upregulation of FnBPs was studied in isogenic mutants of fluoroquinolone-resistant strain RA1 (a topoisomerase IV gyrase double mutant of S. aureus NCTC strain 8325), which exhibited widely different levels of SigB activity, as assessed by quantitative reverse transcription-PCR of their respective sigB and SigB-dependent asp23 transcript levels. These mutants were Tn551 insertion sigB strain TE1 and rsbU+ complemented strain TE2, which exhibited a wild-type SigB operon. Levels of FnBP surface display and fibronectin-mediated adhesion were lower in sigB mutant TE1 or higher in the rsbU+-restored strain TE2 compared to their sigB+ but rsbU parent, strain RA1, exhibiting low levels of SigB activity. Steady-state fnbA and fnbB transcripts levels were similar in strains TE1 and RA1 but increased by 4- and 12-fold, respectively, in strain TE2 compared to those in strain RA1. In contrast, fibronectin-mediated adhesion of strains TE1, RA1, and TE2 was similarly enhanced by growth in the presence of one-eighth the MIC of ciprofloxacin, which led to a significantly higher increase in their fnbB transcript levels compared to the increase in their fnbA transcript levels. Increased SigB levels led to a significant reduction in agr RNAIII; in contrast, it led to a slight increase in sarA transcript levels. In conclusion, upregulation of FnBPs by increased SigB levels and ciprofloxacin exposure in fluoroquinolone-resistant S. aureus occurs via independent pathways whose concerted actions may significantly promote bacterial adhesion and colonization.

* Corresponding author. Mailing address: Division of Infectious Diseases, University Hospitals of Geneva, 24 rue Micheli-du-Crest, CH-1211 Geneva 14, Switzerland. Phone: (4122) 3729826. Fax: (4122) 3729830. E-mail: Pierre.vaudaux{at}hcuge.ch.

{dagger} D.L. and A.R. contributed equally to this work.

Antimicrobial Agents and Chemotherapy, March 2005, p. 916-924, Vol. 49, No. 3
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.3.916-924.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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  • Renzoni, A., Barras, C., Francois, P., Charbonnier, Y., Huggler, E., Garzoni, C., Kelley, W. L., Majcherczyk, P., Schrenzel, J., Lew, D. P., Vaudaux, P. (2006). Transcriptomic and Functional Analysis of an Autolysis-Deficient, Teicoplanin-Resistant Derivative of Methicillin-Resistant Staphylococcus aureus.. Antimicrob. Agents Chemother. 50: 3048-3061 [Abstract] [Full Text]  


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