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Updated: Jun 16, 2026
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
Abstract:
Many endocarditis pathogens activate human platelets and this has been proposed to contribute to virulence. Here we report for the first time that many clinical isolates of Enterococcus faecalis, a common pathogen in infective endocarditis, aggregate human platelets. 84 isolates from human blood and urine were screened for their ability to aggregate platelets from four different donors. Platelet aggregation occurred for between 11 and 65% of isolates depending on the donor. In one donor, a significantly larger proportion of isolates from blood than from urine caused platelet aggregation. Median time to aggregation was 11 min and had a tendency to be shorter for blood isolates as compared to urine isolates. Immunoglobulin G (IgG) was shown to be essential in mediating activation and aggregation. Platelet aggregation could be abolished by an IgG-specific proteinase (IdeS), by an antibody blocking FcRgammaIIa on platelets, or by preabsorption of plasma with an E. faecalis isolate. Fibrinogen binding to bacteria or platelets does not contribute to platelet activation or aggregation under our experimental conditions. These results indicate that platelet activation and aggregation by E. faecalis is dependent on both host and bacterial factors and that it may be involved in the pathogenesis of invasive disease with this organism.
Insights
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.
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.
