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Molecular Pathogenesis

SpyA, a C3-Like ADP-Ribosyltransferase, Contributes to Virulence in a Mouse Subcutaneous Model of Streptococcus pyogenes Infection

Jessica S. Hoff, Mark DeWald, Steve L. Moseley, Carleen M. Collins, Jovanka M. Voyich
B. A. McCormick, Editor
Jessica S. Hoff
1Department of Microbiology, University of Washington, Seattle, Washington
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Mark DeWald
2Veterinary Molecular Biology, Montana State University, Bozeman, Montana
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Steve L. Moseley
1Department of Microbiology, University of Washington, Seattle, Washington
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Carleen M. Collins
1Department of Microbiology, University of Washington, Seattle, Washington
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Jovanka M. Voyich
2Veterinary Molecular Biology, Montana State University, Bozeman, Montana
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  • For correspondence: jovanka@montana.edu
B. A. McCormick
Roles: Editor
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DOI: 10.1128/IAI.01191-10
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ABSTRACT

Streptococcus pyogenes is an important human pathogen with an expansive repertoire of verified and putative virulence factors. Here we demonstrate that a mutant deficient in the production of the streptococcal ADP-ribosyltransferase SpyA generates lesions of reduced size in a subcutaneous mouse infection model. At early stages of infection, when the difference in lesion size is first established, inflamed tissue isolated from lesions of mice infected with spyA mutant bacteria has higher levels of mRNA encoding the chemokines CXCL1 and CCL2 than does tissue isolated from mice infected with wild-type bacteria. In addition, at these early times, the mRNA levels for the gene encoding the intermediate filament vimentin are higher in the mutant-infected tissue. As wound resolution progresses, mRNA levels of the gene encoding matrix metallopeptidase 2 are lower in mutant-infected tissue. Furthermore, we demonstrate that the spyA mutant is internalized more efficiently than wild-type bacteria by HeLa cells. We conclude that SpyA contributes to streptococcal pathogenesis in the mouse subcutaneous infection model. Our observations suggest that the presence of SpyA delays wound healing in this model.

FOOTNOTES

    • Received 8 November 2010.
    • Returned for modification 16 December 2010.
    • Accepted 14 March 2011.
    • Accepted manuscript posted online 21 March 2011.
  • ↵† Supplemental material for this article may be found at http://dx.doi.org/10.1128/IAI.01191-10.

  • Copyright © 2011, American Society for Microbiology
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SpyA, a C3-Like ADP-Ribosyltransferase, Contributes to Virulence in a Mouse Subcutaneous Model of Streptococcus pyogenes Infection
Jessica S. Hoff, Mark DeWald, Steve L. Moseley, Carleen M. Collins, Jovanka M. Voyich
Infection and Immunity May 2011, 79 (6) 2404-2411; DOI: 10.1128/IAI.01191-10

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SpyA, a C3-Like ADP-Ribosyltransferase, Contributes to Virulence in a Mouse Subcutaneous Model of Streptococcus pyogenes Infection
Jessica S. Hoff, Mark DeWald, Steve L. Moseley, Carleen M. Collins, Jovanka M. Voyich
Infection and Immunity May 2011, 79 (6) 2404-2411; DOI: 10.1128/IAI.01191-10
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