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Clinical isolates of Enterococcus faecalis aggregate human platelets.

Rasmussen, Magnus LU ; Johansson, Daniel LU ; Karlsson Söbirk, Sara LU ; Mörgelin, Matthias LU and Shannon, Oonagh LU (2010) In Microbes and Infection 12. p.295-301
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 11minutes and had a tendency to be shorter for blood isolates as compared to urine isolates. Immunoglobulin G (IgG) was... (More)
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 11minutes 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. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
Microbes and Infection
volume
12
pages
295 - 301
publisher
Elsevier
external identifiers
  • wos:000276437600006
  • pmid:20109578
  • scopus:77649275866
ISSN
1769-714X
DOI
10.1016/j.micinf.2010.01.005
language
English
LU publication?
yes
id
7e94e477-50a6-4035-a5e7-e71ee9e7a919 (old id 1540479)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20109578?dopt=Abstract
date added to LUP
2010-02-04 20:47:02
date last changed
2018-05-29 09:25:38
@article{7e94e477-50a6-4035-a5e7-e71ee9e7a919,
  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 11minutes 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.},
  author       = {Rasmussen, Magnus and Johansson, Daniel and Karlsson Söbirk, Sara and Mörgelin, Matthias and Shannon, Oonagh},
  issn         = {1769-714X},
  language     = {eng},
  pages        = {295--301},
  publisher    = {Elsevier},
  series       = {Microbes and Infection},
  title        = {Clinical isolates of Enterococcus faecalis aggregate human platelets.},
  url          = {http://dx.doi.org/10.1016/j.micinf.2010.01.005},
  volume       = {12},
  year         = {2010},
}