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Related Experiment Videos

Platelet aggregation by strains of enterococci.

Y Usui1, Y Ichiman, M Suganuma

  • 1Department of Microbiology, St. Marianna University School of Medicine, Kanagawa, Japan.

Microbiology and Immunology
|January 1, 1991
PubMed
Summary

Enterococcus bacteria can induce platelet aggregation, releasing serotonin. This process requires plasma components and is ion-dependent, not affected by cyclooxygenase inhibitors.

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Area of Science:

  • Microbiology
  • Hematology
  • Immunology

Background:

  • Enterococcus species are opportunistic pathogens.
  • Platelet aggregation plays a crucial role in hemostasis and thrombosis.
  • Understanding bacterial interactions with platelets is important for infection pathogenesis.

Purpose of the Study:

  • To investigate the platelet aggregation capability of Enterococcus faecalis, E. faecium, and E. avium.
  • To elucidate the mechanisms underlying enterococci-induced platelet aggregation.

Main Methods:

  • Testing whole bacterial cells for platelet aggregation.
  • Determining optimal bacteria-to-platelet ratios.
  • Assessing serotonin release during aggregation.
  • Evaluating the effect of inhibitors (EDTA, apyrase, aspirin, indomethacin, quinacrine) and plasma pretreatment (heat, zymosan).

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Main Results:

  • Enterococcus species induced platelet aggregation with varying optimal ratios.
  • Significant serotonin release (65-69%) occurred during aggregation.
  • Aggregation was inhibited by EDTA and apyrase, but not by aspirin, indomethacin, or quinacrine.
  • Plasma pretreatment markedly reduced platelet reactivity.

Conclusions:

  • Enterococci-induced platelet aggregation is an ion-dependent event.
  • The cyclooxygenase pathway is not involved in this aggregation.
  • Plasma components are essential for the reaction between enterococci and platelets.