Platelet Aggregation by Strains of Enterococci

Usui, Yukio; Ichiman, Yoshitoshi; Suganuma, Masaru; Yoshida, Kenichi

doi:10.1111/j.1348-0421.1991.tb01615.x

Cited by 15 publications

(6 citation statements)

References 37 publications

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“…Therefore there appears to be a difference between bacterial strains and species in what constitues their minimum plasma requirements for platelet aggregation. As mentioned earlier, we have shown that NCTC 7863 requires complement for platelet aggregation, as do zymosan (Zucker et al, 1974), certain tumour cells (Pulcinelli et al, 1995), certain monoclonal antibodies (Nomura et al, 1991) and enterococci (Usui et al, 1991), but at present we do not know what proportion of streptococcal strains require complement activation for platelet aggregation. Since aggregation of platelets by some organisms appears to differ in their requirement for complement, and perhaps for antibody, at least part of the mechanism leading up to platelet aggregation differs between strains, although probably all require fibrinogen interaction with GPIIb/IIIa as the final event.…”

Section: Discussionmentioning

confidence: 74%

The role of immunoglobulin G and fibrinogen in platelet aggregation by Streptococcus sanguis

et al. 1997

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Summary.Previous work has shown that the type strain of Streptococcus sanguis, NCTC 7863, induces aggregation of normal platelets by a complement-dependent mechanism. We investigated the roles of IgG and fibrinogen in the aggregation process. Plasma depleted of IgG by passage through protein A-sepharose failed to support platelet aggregation, as did plasma absorbed at 0ЊC with whole bacteria. However, absorption of plasma with a non-aggregating strain of S. sanguis, SK96, did not remove aggregating activity for NCTC 7863. Supplementing 0ЊC-absorbed plasma with purified IgG restored the aggregation supporting activity. A monoclonal antibody to the FcgRII receptor inhibited platelet aggregation by the bacteria, indicating a requirement for bacteria-IgG complexes interacting with the Fc receptor in platelet aggregation. There was a lag time to the onset of platelet aggregation of 7-19 min depending upon the platelet donor, but the length of this lag did not correlate with either total IgG concentration recognizing NCTC 7863 in subjects' plasma, or the concentration any of the four IgG subclasses or with IgG avidity levels.Fibrinogen was shown to bind rapidly to the bacterial cell surface. Monclonal antibody to GPIIb/IIIa, RGDS peptide, and a specific antagonist for the platelet fibrinogen receptor, GPIIb/IIIa, FK633, inhibited platelet aggregation by NCTC 7863, indicating that platelet aggregation is fibrinogen dependent. These data suggest that platelet aggregation by some strains of S. sanguis requires multiple stimuli/agonists, including IgG-Fc receptor interaction, complement and fibrinogen.

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Section: Discussionmentioning

confidence: 74%

The role of immunoglobulin G and fibrinogen in platelet aggregation by Streptococcus sanguis

et al. 1997

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“…This functional redundancy suggests an interaction that is important for the bacteria. Indeed, various other pathogenic bacteria have also been shown to bind to and aggregate platelets, including Streptococcus sanguis (134) (133) (49), Enterococcus faecium, Enterococcus faecalis (139), and Streptococcus pyogenes (80).…”

Section: Antiplatelet Therapymentioning

confidence: 99%

Extracellular fibrinogen binding protein, Efb, from Staphylococcus aureus as an antiplatelet agent in vivo

Shannon¹,

Uekötter²,

Flock³

2005

Thromb Haemost

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Staphylococcus aureus produces and secretes a protein, extracellular fibrinogen binding protein (Efb), which contributes to virulence in wound infection. We have previously shown that Efb is a potent inhibitor of platelet function in vitro. We confirm here that this is also the case in vivo. Pre-treatment with Efb resulted in a significant prolongation of bleeding time in a mouse model. Furthermore, Efb was capable of rescuing animals from death caused by the administration of potent platelet agonists. This antiplatelet effect may explain the retardation of wound healing associated with Efb in S. aureus wound infections. These results are important not only in terms of understanding S. aureus pathogenesis, and consequently identifying new treatment strategies, but also with regard to the development of potential, novel antiplatelet agents for the prevention of thrombosis.

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“…A slower form of aggregation occurs for S. aureus through interactions with specific IgG and complement which induce platelet aggregation after a longer lagtime [6]. Aggregation of rabbit platelets in response to E. faecalis and Enterococcus faecium has been previously described, but the molecular mechanisms involved have not been determined [12]. [13].…”

Section: Introductionmentioning

confidence: 99%

Clinical isolates of Enterococcus faecalis aggregate human platelets

Rasmussen

Johansson

Söbirk

et al. 2010

Microbes and Infection

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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 minutes 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 FcRIIa 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.

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Platelet Aggregation by Strains of Enterococci

Cited by 15 publications

References 37 publications

The role of immunoglobulin G and fibrinogen in platelet aggregation by Streptococcus sanguis

The role of immunoglobulin G and fibrinogen in platelet aggregation by Streptococcus sanguis

Extracellular fibrinogen binding protein, Efb, from Staphylococcus aureus as an antiplatelet agent in vivo

Clinical isolates of Enterococcus faecalis aggregate human platelets

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