Platelet activation and biofilm formation by Aerococcus urinae, an endocarditis causing pathogen.
Shannon, Oonagh LU ; Mörgelin, Matthias LU and Rasmussen, Magnus LU
(2010)
In Infection and Immunity
78(10).
p.4268-4275
- Abstract
- The Gram-positive bacterium Aerococcus urinae can cause infectious endocarditis (IE) in older persons. Biofilm formation and platelet aggregation is believed to contribute to bacterial virulence in IE. Five A. urinae isolates from human blood were shown to form biofilms in vitro and biofilm formation was enhanced by the presence of human plasma. Four of the A. urinae isolates caused platelet aggregation in platelet rich plasma from healthy donors. The Au3 isolate, which induced platelet aggregation in all donors, also activated platelets as determined by flow cytometry. Platelet aggregation was dependent on bacterial protein structures and on platelet activation since it was sensitive to both trypsin and Prostaglandin E1. Plasma proteins... (More)
- The Gram-positive bacterium Aerococcus urinae can cause infectious endocarditis (IE) in older persons. Biofilm formation and platelet aggregation is believed to contribute to bacterial virulence in IE. Five A. urinae isolates from human blood were shown to form biofilms in vitro and biofilm formation was enhanced by the presence of human plasma. Four of the A. urinae isolates caused platelet aggregation in platelet rich plasma from healthy donors. The Au3 isolate, which induced platelet aggregation in all donors, also activated platelets as determined by flow cytometry. Platelet aggregation was dependent on bacterial protein structures and on platelet activation since it was sensitive to both trypsin and Prostaglandin E1. Plasma proteins at the bacterial surface were needed for platelet aggregation and a role for the complement system, fibrinogen, and immunoglobulin G was demonstrated. Complement depleted serum was unable to support platelet aggregation by Au3 and complement blockade using compstatin inhibited platelet activation. Platelet activation by Au3 was inhibited by blocking of the platelet fibrinogen receptor and this isolate was also shown to bind radiolabeled fibrinogen. Removal of IgG from platelet rich plasma by a specific protease inhibited the platelet aggregation induced by A. urinae and blockade of the platelet FcRgammaIIa hindered platelet activation induced by Au3. Convalescent serum from a patient with A. urinae IE transferred the ability of the bacterium to aggregate platelets in an otherwise non-responsive donor. Our results show that A. urinae exhibits virulence strategies of importance for IE. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1665403
- author
- Shannon, Oonagh
LU
; Mörgelin, Matthias
LU
and Rasmussen, Magnus
LU
- organization
- publishing date
- 2010
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Infection and Immunity
- volume
- 78
- issue
- 10
- pages
- 4268 - 4275
- publisher
- American Society for Microbiology
- external identifiers
-
- wos:000282004200019
- pmid:20696834
- scopus:77957737495
- pmid:20696834
- ISSN
- 1098-5522
- DOI
- 10.1128/IAI.00469-10
- language
- English
- LU publication?
- yes
- id
- ddf75875-f032-4b4a-b57b-016477289d58 (old id 1665403)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/20696834?dopt=Abstract
- date added to LUP
- 2016-04-01 10:32:53
- date last changed
- 2024-10-07 07:55:13
@article{ddf75875-f032-4b4a-b57b-016477289d58,
abstract = {{The Gram-positive bacterium Aerococcus urinae can cause infectious endocarditis (IE) in older persons. Biofilm formation and platelet aggregation is believed to contribute to bacterial virulence in IE. Five A. urinae isolates from human blood were shown to form biofilms in vitro and biofilm formation was enhanced by the presence of human plasma. Four of the A. urinae isolates caused platelet aggregation in platelet rich plasma from healthy donors. The Au3 isolate, which induced platelet aggregation in all donors, also activated platelets as determined by flow cytometry. Platelet aggregation was dependent on bacterial protein structures and on platelet activation since it was sensitive to both trypsin and Prostaglandin E1. Plasma proteins at the bacterial surface were needed for platelet aggregation and a role for the complement system, fibrinogen, and immunoglobulin G was demonstrated. Complement depleted serum was unable to support platelet aggregation by Au3 and complement blockade using compstatin inhibited platelet activation. Platelet activation by Au3 was inhibited by blocking of the platelet fibrinogen receptor and this isolate was also shown to bind radiolabeled fibrinogen. Removal of IgG from platelet rich plasma by a specific protease inhibited the platelet aggregation induced by A. urinae and blockade of the platelet FcRgammaIIa hindered platelet activation induced by Au3. Convalescent serum from a patient with A. urinae IE transferred the ability of the bacterium to aggregate platelets in an otherwise non-responsive donor. Our results show that A. urinae exhibits virulence strategies of importance for IE.}},
author = {{Shannon, Oonagh and Mörgelin, Matthias and Rasmussen, Magnus}},
issn = {{1098-5522}},
language = {{eng}},
number = {{10}},
pages = {{4268--4275}},
publisher = {{American Society for Microbiology}},
series = {{Infection and Immunity}},
title = {{Platelet activation and biofilm formation by Aerococcus urinae, an endocarditis causing pathogen.}},
url = {{http://dx.doi.org/10.1128/IAI.00469-10}},
doi = {{10.1128/IAI.00469-10}},
volume = {{78}},
year = {{2010}},
}