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Infection and Immunity, August 2006, p. 4849-4855, Vol. 74, No. 8
0019-9567/06/$08.00+0     doi:10.1128/IAI.00230-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Comparative Antibody-Mediated Phagocytosis of Staphylococcus epidermidis Cells Grown in a Biofilm or in the Planktonic State

Nuno Cerca,1,2 Kimberly K. Jefferson,2,3 Rosario Oliveira,1 Gerald B. Pier,2* and Joana Azeredo1

Centro de Engenharia Biológica, Universidade do Minho, Braga, Portugal,1 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts,2 Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia3

Received 10 February 2006/ Returned for modification 18 March 2006/ Accepted 25 May 2006

Staphylococcus epidermidis is an important cause of nosocomial infections. Virulence is attributable to elaboration of biofilms on medical surfaces that protect the organisms from immune system clearance. Even though leukocytes can penetrate biofilms, they fail to phagocytose and kill bacteria. The properties that make biofilm bacteria resistant to the immune system are not well characterized. In order to better understand the mechanisms of resistance of bacteria in biofilms to the immune system, we evaluated antibody penetration throughout the biofilm and antibody-mediated phagocytic killing of planktonic versus biofilm cells of S. epidermidis by using a rabbit antibody to poly-N-acetylglucosamine (PNAG). These antibodies are opsonic and protect against infection with planktonic cells of PNAG-positive Staphylococcus aureus and S. epidermidis. Antibody to PNAG readily penetrated the biofilm and bound to the same areas in the biofilm as did wheat germ agglutinin, a lectin known to bind to components of staphylococcal biofilms. However, biofilm cells were more resistant to opsonic killing than their planktonic counterparts in spite of producing more PNAG per cell than planktonic cells. Biofilm extracts inhibited opsonic killing mediated by antibody to PNAG, suggesting that the PNAG antigen within the biofilm matrix prevents antibody binding close to the bacterial cell surface, which is needed for efficient opsonic killing. Increased resistance of biofilm cells to opsonic killing mediated by an otherwise protective antibody was due not to a biofilm-specific phenotype but rather to high levels of antigen within the biofilm that prevented bacterial opsonization by the antibody.

* Corresponding author. Mailing address: Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, 181 Longwood Ave., Boston, MA 02115. Phone: (617) 525-2269. Fax: (617) 525-2510. E-mail: gpier{at}channing.harvard.edu.

Editor: J. T. Barbieri

Infection and Immunity, August 2006, p. 4849-4855, Vol. 74, No. 8
0019-9567/06/$08.00+0     doi:10.1128/IAI.00230-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Shahrooei, M., Hira, V., Stijlemans, B., Merckx, R., Hermans, P. W. M., Van Eldere, J. (2009). Inhibition of Staphylococcus epidermidis Biofilm Formation by Rabbit Polyclonal Antibodies against the SesC Protein. Infect. Immun. 77: 3670-3678 [Abstract] [Full Text]  
  • Brady, R. A., Leid, J. G., Kofonow, J., Costerton, J. W., Shirtliff, M. E. (2007). Immunoglobulins to Surface-Associated Biofilm Immunogens Provide a Novel Means of Visualization of Methicillin-Resistant Staphylococcus aureus Biofilms. Appl. Environ. Microbiol. 73: 6612-6619 [Abstract] [Full Text]  


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