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M protein-mediated plasminogen binding is essential for the virulence of an invasive Streptococcus pyogenes isolate

M L Sanderson-Smith1, K Dinkla, J N Cole

  • 1School of Biological Sciences, University of Wollongong, Wollongong, NSW, 2522, Australia.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|May 10, 2008
PubMed

Insights

Group A Streptococcus (GAS) uses human plasmin to cause invasive disease. Blocking plasminogen binding to the M protein Prp significantly reduced GAS virulence in a mouse model.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Group A Streptococcus (GAS; Streptococcus pyogenes) is a significant human pathogen.
  • GAS causes invasive diseases, particularly in regions like Australia's Northern Territory.
  • The human protease plasmin is implicated in GAS pathogenesis.

Purpose of the Study:

  • To investigate the role of plasminogen binding by the GAS M protein Prp in virulence.
  • To determine how cell surface plasmin acquisition contributes to GAS invasive disease.

Main Methods:

  • Engineered an isogenic mutant (NS88.2prp) of GAS strain NS88.2 by altering key plasminogen-binding residues in the Prp protein.
  • Constructed a reverse complemented strain (NS88.2prpRC) with wild-type Prp sequence.
  • Assessed plasminogen binding and cell surface plasmin activity during growth in human plasma.
  • Evaluated GAS virulence using a humanized plasminogen mouse model of invasive infection.

Main Results:

  • The NS88.2prp mutant showed significantly reduced binding of human plasminogen compared to wild-type and NS88.2prpRC strains.
  • The mutant exhibited diminished accumulation of cell surface plasmin activity.
  • Impaired plasminogen binding and surface plasmin activity correlated with reduced GAS virulence in the mouse model.

Conclusions:

  • Plasminogen binding by the GAS M protein Prp is critical for acquiring cell surface plasmin activity.
  • This plasmin activity is essential for the virulence of Group A Streptococcus in invasive infections.

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