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Infection and Immunity, May 2008, p. 2044-2050, Vol. 76, No. 5
0019-9567/08/$08.00+0     doi:10.1128/IAI.00035-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Staphylococcus aureus CcpA Affects Biofilm Formation{triangledown}

Kati Seidl,1 Christiane Goerke,2 Christiane Wolz,2 Dietrich Mack,3 Brigitte Berger-Bächi,1 and Markus Bischoff1,4*

Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland,1 Institute for Medical Microbiology and Hygiene, University Hospital—Tübingen, Tübingen, Germany,2 University of Wales—Swansea, Swansea, United Kingdom,3 Institute of Medical Microbiology and Hygiene, University of Saarland Hospital, Homburg/Saar, Germany4

Received 10 January 2008/ Returned for modification 18 February 2008/ Accepted 6 March 2008

Biofilm formation in Staphylococcus aureus under in vitro growth conditions is generally promoted by high concentrations of sugar and/or salts. The addition of glucose to routinely used complex growth media triggered biofilm formation in S. aureus strain SA113. Deletion of ccpA, coding for the catabolite control protein A (CcpA), which regulates gene expression in response to the carbon source, abolished the capacity of SA113 to form a biofilm under static and flow conditions, while still allowing primary attachment to polystyrene surfaces. This suggested that CcpA mainly affects biofilm accumulation and intercellular aggregation. trans-Complementation of the mutant with the wild-type ccpA allele fully restored the biofilm formation. The biofilm produced by SA113 was susceptible to sodium metaperiodate, DNase I, and proteinase K treatment, indicating the presence of polysaccharide intercellular adhesin (PIA), protein factors, and extracellular DNA (eDNA). The investigation of several factors which were reported to influence biofilm formation in S. aureus (arlRS, mgrA, rbf, sarA, atl, ica, citZ, citB, and cidABC) showed that CcpA up-regulated the transcription of cidA, which was recently shown to contribute to eDNA production. Moreover, we showed that CcpA increased icaA expression and PIA production, presumably over the down-regulation of the tricarboxylic acid cycle genes citB and citZ.

* Corresponding author. Mailing address: Institute of Medical Microbiology and Hygiene, University of Saarland Hospital, 66421 Homburg/Saar, Germany. Phone: 49 6841 162 39 63. Fax: 49 6841 162 39 85. E-mail: markus.bischoff{at}uniklinikum-saarland.de

{triangledown} Published ahead of print on 10 March 2008.

Editor: A. J. Bäumler

Infection and Immunity, May 2008, p. 2044-2050, Vol. 76, No. 5
0019-9567/08/$08.00+0     doi:10.1128/IAI.00035-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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