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Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells
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Activation of TAFI on the surface of Streptococcus pyogenes evokes inflammatory reactions by modulating the

Sara H Bengtson1, Caroline Sandén, Matthias Mörgelin

  • 1Department of Clinical Sciences, Section for Clinical and Experimental Infection Medicine, Lund University, Lund, Sweden. Sara.Mattsson@med.lu.se

Journal of Innate Immunity
|April 9, 2010
PubMed

Insights

Streptococcus pyogenes uses thrombin-activatable fibrinolysis inhibitor (TAFI) to alter host inflammation. This pathogen-bound TAFI converts bradykinin (BK) into a B1 receptor agonist, potentially prolonging inflammation.

Area of Science:

  • Microbiology
  • Immunology
  • Biochemistry

Background:

  • Bacterial virulence involves modulating host responses.
  • The kallikrein/kinin system plays a role in inflammation and infection.

Purpose of the Study:

  • To investigate the role of Streptococcus pyogenes in modulating the kallikrein/kinin system.
  • To elucidate the mechanism by which S. pyogenes influences host inflammatory responses.

Main Methods:

  • Investigated the interaction between S. pyogenes and thrombin-activatable fibrinolysis inhibitor (TAFI).
  • Analyzed the effect of TAFI on the contact system and bradykinin (BK) processing.
  • Assessed the impact of bacterial supernatants on inflammatory cytokine production and receptor expression.

Main Results:

  • S. pyogenes recruits and activates TAFI on its surface.
  • TAFI processes BK into a kinin B(1) receptor (B1R) agonist.
  • Bacterial supernatants induce inflammatory cytokines that upregulate B1R on fibroblasts.

Conclusions:

  • Streptococci-bound TAFI plays a novel role in processing BK to a B1R agonist.
  • This mechanism may redirect acute inflammation towards a chronic state.
  • Understanding this interaction is crucial for developing new therapeutic strategies against S. pyogenes infections.

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