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Journal of Bacteriology, February 2009, p. 832-843, Vol. 191, No. 3
0021-9193/09/$08.00+0     doi:10.1128/JB.01222-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Protein A-Mediated Multicellular Behavior in Staphylococcus aureus{triangledown}

Nekane Merino,1 Alejandro Toledo-Arana,1 Marta Vergara-Irigaray,1 Jaione Valle,1 Cristina Solano,1 Enrique Calvo,2 Juan Antonio Lopez,2 Timothy J. Foster,4 José R. Penadés,3 and Iñigo Lasa1*

Instituto de Agrobiotecnología, Universidad Pública de Navarra-CSIC-Gobierno de Navarra, 31006 Pamplona, Spain,1 Unidad de Proteómica, Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, 28029 Madrid, Spain,2 Instituto Valenciano de Investigaciones Agrarias and Cardenal Herrera-CEU University, 46113 Moncada, Valencia, Spain,3 Department of Microbiology, Moyne Institute of Preventive Medicine, University of Dublin, Trinity College, Dublin, Ireland4

Received 1 September 2008/ Accepted 19 November 2008

The capacity of Staphylococcus aureus to form biofilms on host tissues and implanted medical devices is one of the major virulence traits underlying persistent and chronic infections. The matrix in which S. aureus cells are encased in a biofilm often consists of the polysaccharide intercellular adhesin (PIA) or poly-N-acetyl glucosamine (PNAG). However, surface proteins capable of promoting biofilm development in the absence of PIA/PNAG exopolysaccharide have been described. Here, we used two-dimensional nano-liquid chromatography and mass spectrometry to investigate the composition of a proteinaceous biofilm matrix and identified protein A (spa) as an essential component of the biofilm; protein A induced bacterial aggregation in liquid medium and biofilm formation under standing and flow conditions. Exogenous addition of synthetic protein A or supernatants containing secreted protein A to growth media induced biofilm development, indicating that protein A can promote biofilm development without being covalently anchored to the cell wall. Protein A-mediated biofilm formation was completely inhibited in a dose-dependent manner by addition of serum, purified immunoglobulin G, or anti-protein A-specific antibodies. A murine model of subcutaneous catheter infection unveiled a significant role for protein A in the development of biofilm-associated infections, as the amount of protein A-deficient bacteria recovered from the catheter was significantly lower than that of wild-type bacteria when both strains were used to coinfect the implanted medical device. Our results suggest a novel role for protein A complementary to its known capacity to interact with multiple immunologically important eukaryotic receptors.

* Corresponding author. Mailing address: Instituto de Agrobiotecnología, Universidad Pública de Navarra, Pamplona 31006, Spain. Phone: 34 948 168007. Fax: 34 948 232191. E-mail: ilasa{at}unavarra.es

{triangledown} Published ahead of print on 1 December 2008.

Journal of Bacteriology, February 2009, p. 832-843, Vol. 191, No. 3
0021-9193/09/$08.00+0     doi:10.1128/JB.01222-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Baum, C., Haslinger-Loffler, B., Westh, H., Boye, K., Peters, G., Neumann, C., Kahl, B. C. (2009). Non-spa-Typeable Clinical Staphylococcus aureus Strains Are Naturally Occurring Protein A Mutants. J. Clin. Microbiol. 47: 3624-3629 [Abstract] [Full Text]  
  • Vergara-Irigaray, M., Valle, J., Merino, N., Latasa, C., Garcia, B., Ruiz de los Mozos, I., Solano, C., Toledo-Arana, A., Penades, J. R., Lasa, I. (2009). Relevant Role of Fibronectin-Binding Proteins in Staphylococcus aureus Biofilm-Associated Foreign-Body Infections. Infect. Immun. 77: 3978-3991 [Abstract] [Full Text]  


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