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Related Experiment Videos

Trigger for group A streptococcal M1T1 invasive disease.

Jason N Cole1, Jason D McArthur, Fiona C McKay

  • 1School of Biological Sciences, University of Wollongong, Wollongong, New South Wales, 2522, Australia.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|June 23, 2006
PubMed
Summary

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Group A Streptococcus M1T1 bacteria spread systemically by hijacking the human plasminogen system. Reduced SpeB protease activity allows M1T1 bacteria to accumulate plasmin, initiating invasive disease.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Molecular Biology

Background:

  • The globally prevalent Streptococcus pyogenes M1T1 clone causes severe invasive human diseases.
  • The mechanism of transition from localized infection to systemic disease remains unclear.
  • Invasive M1T1 isolates exhibit lower cysteine protease SpeB expression than those from localized infections.

Purpose of the Study:

  • To investigate the role of the human plasminogen system in Streptococcus pyogenes M1T1 systemic infection.
  • To elucidate the function of SpeB protease in M1T1 pathogenesis and dissemination.

Main Methods:

  • Comparison of wild-type M1T1 strain 5448 with an isogenic delta speB mutant.
  • Incubation in human plasma to assess surface plasmin activity.

Related Experiment Videos

  • Infection of humanized plasminogen transgenic mice to evaluate virulence and SpeB expression.

    • Main Results:

    • The delta speB mutant accumulated 75-fold more human plasmin activity on its surface compared to the wild-type strain.
    • Human plasminogen was essential for M1T1 virulence in vivo.
    • M1T1 isolates from systemic infections showed reduced SpeB levels.

    Conclusions:

    • The human plasminogen system is critical for initiating Streptococcus pyogenes M1T1 systemic disease.
    • SpeB protease is necessary for M1T1 survival at the infection site but hinders plasminogen interaction.
    • Loss of SpeB in a bacterial subpopulation facilitates plasmin accumulation and systemic spread.