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Severe streptococcal infection is associated with M protein-induced platelet activation and thrombus formation.

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Author

Summary, in English

Disturbed haemostasis is a central finding in severe Streptococcus pyogenes infection. In particular, microthrombi are found both at the local site of infection and at distant sites. Platelets are responsible for maintaining vascular function and haemostasis. We report here that M1 protein of S. pyogenes triggers immune-mediated platelet activation and thrombus formation. M1 protein is released from the bacterial surface and forms complexes with plasma fibrinogen. These complexes bind to the fibrinogen receptor on resting platelets. When these complexes also contain immunoglobulin G (IgG) against M1 protein, this will engage the Fc receptor on the platelets and activation will occur. Activation of the platelets leads to platelet aggregation and the generation of platelet-rich thrombi. Neutrophils and monocytes are in turn activated by the platelets. Platelet thrombi are deposited in the microvasculature, and aggregated platelets, IgG and M1 protein colocalize in biopsies from patients diagnosed with S. pyogenes toxic shock syndrome. This chain of events results in a procoagulant and pro-inflammatory state typical of severe S. pyogenes infection.

Publishing year

2007

Language

English

Pages

1147-1157

Publication/Series

Molecular Microbiology

Volume

65

Issue

5

Document type

Journal article

Publisher

Wiley-Blackwell

Topic

  • Microbiology in the medical area

Status

Published

Research group

  • epIgG
  • SEBRA Sepsis and Bacterial Resistance Alliance

ISBN/ISSN/Other

  • ISSN: 1365-2958