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Infection and Immunity, September 2006, p. 5319-5324, Vol. 74, No. 9
0019-9567/06/$08.00+0     doi:10.1128/IAI.00543-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The Contribution of PspC to Pneumococcal Virulence Varies between Strains and Is Accomplished by Both Complement Evasion and Complement-Independent Mechanisms

Alison R. Kerr,¹ Gavin K. Paterson,^1, Jackie McCluskey,¹ Francesco Iannelli,² Marco R. Oggioni,² Gianni Pozzi,² and Tim J. Mitchell^1*

Division of Infection and Immunity, IBLS, University of Glasgow, Glasgow, G12 8TA, United Kingdom,¹ Laboratory of Molecular Microbiology and Biotechnology, Department of Molecular Biology, University of Siena, 53100 Siena, Italy²

Received 4 April 2006/ Returned for modification 16 May 2006/ Accepted 26 June 2006

Pneumococcal surface protein C (PspC) is a virulence factor of Streptococcus pneumoniae previously shown to play a role in bacterial adherence, invasion, and evasion of complement. We investigated the role of this protein in our murine models of pneumococcal pneumonia with different pneumococcal strains. The deletion of pspC in strains of serotypes 2, 3, and 19F did not significantly alter host survival times in the pneumonia model. In contrast, pspC deletion significantly reduced the virulence of the serotype 4 strain, TIGR4, in both the pneumonia and bacteremia models. Therefore, pspC is a systemic and pulmonary virulence determinant for S. pneumoniae, but its effects are influenced by the pneumococcal strain. Finally, pneumonia infection of complement-deficient (C3^–/–) mice enhanced pspC virulence, illustrating that PspC-mediated complement evasion contributes to virulence. However, other functions of PspC also contribute to virulence, as demonstrated by the finding that the pspC-deficient TIGR4 mutant was still attenuated relative to the wild-type parent, even in the absence of C3.

Editor: J. N. Weiser

Present address: Biomedical Sciences, DSTL, Porton Down, Salisbury, SP4 0JQ, United Kingdom.

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