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Platelet Activation and Aggregation Induced by Streptococcus bovis/Streptococcus equinus Complex.

Gustav Pernow1, Oonagh Shannon2, Jonas Öberg1

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Summary

The Streptococcus bovis/Streptococcus equinus complex (SBSEC) can activate and aggregate human platelets, a key step in infective endocarditis (IE). This interaction is IgG and Fc-receptor dependent, suggesting a potential therapeutic target for IE prevention and treatment.

Keywords:
IgG-Fc-receptorStreptococcus bovis/Streptococcus equinus complexbacteria-platelet interactionsinfective endocarditisplatelet activationsubspecies

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Area of Science:

  • Microbiology
  • Immunology
  • Cardiovascular Research

Background:

  • The Streptococcus bovis/Streptococcus equinus complex (SBSEC) is a significant cause of infective endocarditis (IE).
  • Bacterial activation and aggregation of platelets are crucial virulence mechanisms in IE pathogens.
  • Limited research exists on SBSEC's interaction with platelets and the underlying mechanisms.

Purpose of the Study:

  • To investigate the capacity of SBSEC isolates to induce platelet activation and aggregation.
  • To elucidate the mechanisms involved in SBSEC-mediated platelet responses.
  • To identify potential therapeutic targets for SBSEC-related IE.

Main Methods:

  • Collected 26 SBSEC isolates from bacteremia cases.
  • Studied platelet interactions using platelet-rich plasma (PRP) from human donors.
  • Assessed aggregation via light-transmission aggregometry and activation via CD62P expression using flow cytometry.
  • Utilized inhibitors and IgG cleavage to determine the role of Fc-receptors and IgG.

Main Results:

  • Twenty-two of 26 SBSEC isolates induced platelet aggregation in at least one donor.
  • Isolate SL1 demonstrated rapid aggregation (50% in 70s).
  • Platelet activation and aggregation were abolished by blocking Fc-receptors or cleaving IgG, indicating an IgG-Fc-receptor dependent pathway.
  • Bacteria-induced platelet aggregation was transferable via serum, suggesting soluble factors are involved.

Conclusions:

  • SBSEC isolates commonly induce platelet aggregation, a host-dependent phenomenon.
  • The IgG-Fc-receptor pathway is essential for SBSEC-mediated platelet activation and aggregation.
  • This pathway represents a potential therapeutic target for preventing and treating IE caused by SBSEC.