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Infection and Immunity, July 2002, p. 3865-3873, Vol. 70, No. 7
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.7.3865-3873.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Increased Virulence of a Fibronectin-Binding Protein Mutant of Staphylococcus aureus in a Rat Model of Pneumonia

Mary C. McElroy,1* David J. Cain,1 Christine Tyrrell,1 Timothy J. Foster,2 and Christopher Haslett1

Rayne Laboratory, Respiratory Medicine, University of Edinburgh, Scotland,1 Department of Microbiology, Moyne Institute of Preventive Medicine, Trinity College, Dublin, Ireland2

Received 31 October 2001/ Returned for modification 3 January 2002/ Accepted 25 March 2002

Fibronectin-binding proteins mediate Staphylococcus aureus internalization into nonphagocytic cells in vitro. We have investigated whether fibronectin-binding proteins are virulence factors in the pathogenesis of pneumonia by using S. aureus strain 8325-4 and isogenic mutants in which fibronectin-binding proteins were either deleted (DU5883) or overexpressed [DU5883(pFnBPA4)]. We first demonstrated that fibronectin-binding proteins mediate S. aureus internalization into alveolar epithelial cells in vitro and that S. aureus internalization into alveolar epithelial cells requires actin rearrangement and protein kinase activity. Second, we established a rat model of S. aureus-induced pneumonia and measured lung injury and bacterial survival at 24 and 96 h postinoculation. S. aureus growth and the extent of lung injury were both increased in rats inoculated with the deletion mutant (DU5883) in comparison with rats inoculated with the wild-type (8325-4) and the fibronectin-binding protein-overexpressing strain DU5883(pFnBPA4) at 24 h postinfection. Morphological evaluation of infected lungs at the light and electron microscopic levels demonstrated that S. aureus was present within neutrophils from both 8325-4- and DU5883-inoculated lungs. Our data suggest that fibronectin-binding protein-mediated internalization into alveolar epithelial cells is not a virulence mechanism in a rat model of pneumonia. Instead, our data suggest that fibronectin-binding proteins decrease the virulence of S. aureus in pneumonia.

* Corresponding author. Mailing address: Department of Pathology, University of Edinburgh, Teviot Place, Edinburgh, Scotland EH8 9AG. Phone: 0131-65-1324. Fax: 0131-650-4384. E-mail: mmcelroy{at}ed.ac.uk.

Editor: B. B. Finlay

Infection and Immunity, July 2002, p. 3865-3873, Vol. 70, No. 7
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.7.3865-3873.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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