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Infection and Immunity, May 2002, p. 2526-2534, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2526-2534.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Role of Pneumococcal Surface Protein C in Nasopharyngeal Carriage and Pneumonia and Its Ability To Elicit Protection against Carriage of Streptococcus pneumoniae

Priya Balachandran,* Alexis Brooks-Walter,,{dagger} Anni Virolainen-Julkunen,,{ddagger} Susan K. Hollingshead, and David E. Briles

Department of Microbiology, The University of Alabama at Birmingham, Birmingham, Alabama 35294

Received 6 September 2001/ Returned for modification 24 October 2001/ Accepted 25 January 2002

Previous studies suggested that PspC is important in adherence and colonization within the nasopharynx. In this study, we conducted mutational studies to further identify the role PspC plays in the pathogenesis of pneumococci. pspC and/or pspA was insertionally inactivated in a serotype 2 Streptococcus pneumoniae strain and in a serotype 19 S. pneumoniae strain. In the mouse colonization model, pneumococcal strains with mutations in pspC were significantly attenuated in their abilities to colonize. In a mouse pneumonia model, strains with mutations in pspC were unable to infect or multiply within the lung. Using reverse transcriptase PCR we were able to demonstrate that pspC is actively transcribed in vivo, when the bacteria are growing in the nasal cavity and in the lungs. In the bacteremia model, a strain mutated for pspC alone behaved like the wild type, but the absence of both pspC and pspA caused accelerated clearance of the bacteria. Intranasal immunization with PspC with cholera toxin subunit B as an adjuvant protected against intranasal challenge. Evidence was also obtained that revertants that spontaneously acquired PspC expression could multiply and colonize the nasal tissue. This latter finding strongly indicates that pneumococci are actively metabolizing and growing while in the nasopharynx.

* Corresponding author. Present address: Department of Medicine, University of California, San Francisco, San Francisco, CA 94143. Phone: (205) 934-1880. Fax: (205) 934-0605. E-mail: priyab@itsa.ucsf.edu.

Editor: E. I. Tuomanen

{dagger} Present address: Department of Biology, Florida A&M University, Tallahassee, FL 32307.

{ddagger} Present address: Department of Bacteriology and Immunology, Haartman Institute and Helsinki University Central Hospital, 00014 University of Helsinki, Finland.

Infection and Immunity, May 2002, p. 2526-2534, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2526-2534.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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