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Molecular co-operation between protein PAM and streptokinase for plasmin acquisition by Streptococcus pyogenes

U Ringdahl1, M Svensson, A C Wistedt

  • 1Department of Medical Microbiology, University of Lund, S-223 62 Lund, Sweden.

Insights

Group A streptococci use surface protein PAM to bind plasminogen, enabling plasmin formation. This process, dependent on streptokinase, facilitates bacterial invasion of host tissues.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Bacterial surface-associated plasmin formation aids invasion but lacks clear molecular understanding.
  • Group A streptococci (GAS) utilize surface proteins to interact with host factors.
  • Plasminogen binding is a key step in bacterial plasmin generation.

Purpose of the Study:

  • To identify the molecular components essential for plasmin generation on GAS.
  • To investigate the role of the M-like protein PAM in plasminogen binding and activation.
  • To elucidate the interaction between surface proteins and secreted factors in bacterial plasmin acquisition.

Main Methods:

  • Genetic engineering of M-like proteins (Arp4 and PAM) in *Escherichia coli* and GAS.
  • Construction of chimeric proteins by incorporating plasminogen-binding repeats from PAM into Arp4.
  • Assessing plasminogen and plasmin binding to engineered proteins and bacterial strains.
  • Evaluating plasminogen activation on streptococcal surfaces with and without functional streptokinase.

Main Results:

  • Chimeric Arp/PAM proteins containing PAM repeats bound both plasminogen and plasmin.
  • GAS strains expressing Arp/PAM constructs efficiently bound plasminogen.
  • Streptococci expressing PAM or Arp/PAM acquired surface-bound plasmin in the presence of plasminogen.
  • Plasminogen activation was blocked in strains with inactivated streptokinase but restored by exogenous streptokinase.

Conclusions:

  • The M-like protein PAM is crucial for bacterial plasminogen binding.
  • Surface-bound PAM and secreted streptokinase cooperate for bacterial plasmin acquisition.
  • This mechanism enhances bacterial invasion by facilitating the formation of a host protease on the bacterial surface.

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