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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1540479
- author
- Rasmussen, Magnus
LU
; Johansson, Daniel
LU
; Karlsson Söbirk, Sara
LU
; Mörgelin, Matthias
LU
and Shannon, Oonagh
LU
- organization
- publishing date
- 2010
- 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
- 2016-04-04 08:22:53
- date last changed
- 2022-03-23 02:26:03
@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 = {{https://lup.lub.lu.se/search/files/5177837/1567567.pdf}},
doi = {{10.1016/j.micinf.2010.01.005}},
volume = {{12}},
year = {{2010}},
}