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Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

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Related Experiment Video

Updated: Jun 16, 2026

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

Clinical isolates of Enterococcus faecalis aggregate human platelets.

Magnus Rasmussen1, Daniel Johansson, Sara K Söbirk

  • 1Department of Clinical Sciences, Division of Infection Medicine, Lund University, Lund, Sweden. magnus.rasmussen@med.lu.se

Microbes and Infection
|January 30, 2010
PubMed
Summary
This summary is machine-generated.

Enterococcus faecalis, an endocarditis pathogen, aggregates human platelets, a process crucial for virulence. This platelet aggregation is mediated by Immunoglobulin G (IgG) and involves both host and bacterial factors.

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Published on: October 27, 2009

Area of Science:

  • Microbiology
  • Immunology
  • Hematology

Background:

  • Platelet activation by pathogens is linked to virulence in infective endocarditis.
  • Enterococcus faecalis is a significant cause of infective endocarditis.

Purpose of the Study:

  • To investigate the ability of clinical isolates of Enterococcus faecalis to aggregate human platelets.
  • To elucidate the mechanisms underlying E. faecalis-induced platelet aggregation.

Main Methods:

  • Screening of 84 clinical isolates of E. faecalis for platelet aggregation.
  • Testing the role of Immunoglobulin G (IgG), Fc receptor gamma IIa (FcRgammaIIa), and fibrinogen in aggregation.
  • Utilizing an IgG-specific proteinase (IdeS) and blocking antibodies.

Main Results:

  • A variable proportion of E. faecalis isolates (11-65%) induced platelet aggregation, donor-dependent.
  • Blood isolates showed a higher propensity for platelet aggregation compared to urine isolates.
  • Platelet aggregation was dependent on Immunoglobulin G (IgG) and mediated via FcRgammaIIa, not fibrinogen.

Conclusions:

  • Enterococcus faecalis activates and aggregates human platelets, suggesting a role in virulence.
  • The interaction involves both bacterial and host factors, specifically IgG and platelet FcRgammaIIa.
  • This finding provides insights into the pathogenesis of invasive E. faecalis infections.