Faculty Collaboration Database

SpyA, a C3-like ADP-ribosyltransferase, contributes to virulence in a mouse subcutaneous model of Streptococcus pyogenes infection. Infect Immun 2011 Jun;79(6):2404-11

Date

03/23/2011

Pubmed ID

21422178

Pubmed Central ID

PMC3125853

DOI

10.1128/IAI.01191-10

Scopus ID

2-s2.0-79959412072 (requires institutional sign-in at Scopus site)   18 Citations

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.

Author List

Hoff JS, DeWald M, Moseley SL, Collins CM, Voyich JM

Author

Jessica Hoff PhD Assistant Professor in the Pathology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

ADP Ribose Transferases
Animals
Blotting, Western
Chemokine CCL2
Chemokine CXCL1
Disease Models, Animal
Epithelial Cells
Female
HeLa Cells
Humans
Mice
Neutrophils
Reverse Transcriptase Polymerase Chain Reaction
Streptococcal Infections
Streptococcus pyogenes
Virulence Factors