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Platelet and neutrophil responses to gram positive pathogens in patients with bacteremic infection.

Johansson, Daniel LU ; Shannon, Oonagh LU and Rasmussen, Magnus LU (2011) In PLoS ONE 6(11).
Abstract
BACKGROUND:

Many Gram-positive pathogens aggregate and activate platelets in vitro and this has been proposed to contribute to virulence. Platelets can also form complexes with neutrophils but little is however known about platelet and platelet-neutrophil responses in bacterial infection.



METHODOLOGY/PRINCIPAL FINDINGS:

We added isolates of Gram-positive bacteria from 38 patients with a bacteremic infection to blood drawn from the same patient. Aggregometry and flow cytometry were used to assess platelet aggregation and to quantify activation of platelets, neutrophils, and platelet-neutrophils complexes (PNCs) induced by the bacteria. Fifteen healthy persons served as controls. Most isolates of... (More)
BACKGROUND:

Many Gram-positive pathogens aggregate and activate platelets in vitro and this has been proposed to contribute to virulence. Platelets can also form complexes with neutrophils but little is however known about platelet and platelet-neutrophil responses in bacterial infection.



METHODOLOGY/PRINCIPAL FINDINGS:

We added isolates of Gram-positive bacteria from 38 patients with a bacteremic infection to blood drawn from the same patient. Aggregometry and flow cytometry were used to assess platelet aggregation and to quantify activation of platelets, neutrophils, and platelet-neutrophils complexes (PNCs) induced by the bacteria. Fifteen healthy persons served as controls. Most isolates of Staphylococcus aureus, beta hemolytic streptococci, and Enterococcus faecalis induced aggregation of platelets from their respective hosts, whereas pneumococci failed to do so. S. aureus isolates induced platelet aggregation more rapidly in patients than in controls, whereas platelet activation by S. aureus was lower in patients than in controls. PNCs were more abundant in baseline samples from patients than in healthy controls and most bacterial isolates induced additional PNC formation and neutrophil activation.



CONCLUSION/SIGNIFICANCE:

We have demonstrated for the first time that bacteria isolated from patients with Gram-positive bacteremia can induce platelet activation and aggregation, PNC formation, and neutrophil activation in the same infected host. This underlines the significance of these interactions during infection, which could be a target for future therapies in sepsis. (Less)
Please use this url to cite or link to this publication:
author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
PLoS ONE
volume
6
issue
11
article number
e26928
publisher
Public Library of Science (PLoS)
external identifiers
  • wos:000298166300003
  • pmid:22140434
  • scopus:82255169339
  • pmid:22140434
ISSN
1932-6203
DOI
10.1371/journal.pone.0026928
language
English
LU publication?
yes
id
8b4ab6b4-74ad-479f-bab1-331b0b189b4e (old id 2274584)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22140434?dopt=Abstract
date added to LUP
2016-04-04 09:07:52
date last changed
2022-04-23 19:08:56
@article{8b4ab6b4-74ad-479f-bab1-331b0b189b4e,
  abstract     = {{BACKGROUND:<br/><br>
Many Gram-positive pathogens aggregate and activate platelets in vitro and this has been proposed to contribute to virulence. Platelets can also form complexes with neutrophils but little is however known about platelet and platelet-neutrophil responses in bacterial infection.<br/><br>
<br/><br>
METHODOLOGY/PRINCIPAL FINDINGS:<br/><br>
We added isolates of Gram-positive bacteria from 38 patients with a bacteremic infection to blood drawn from the same patient. Aggregometry and flow cytometry were used to assess platelet aggregation and to quantify activation of platelets, neutrophils, and platelet-neutrophils complexes (PNCs) induced by the bacteria. Fifteen healthy persons served as controls. Most isolates of Staphylococcus aureus, beta hemolytic streptococci, and Enterococcus faecalis induced aggregation of platelets from their respective hosts, whereas pneumococci failed to do so. S. aureus isolates induced platelet aggregation more rapidly in patients than in controls, whereas platelet activation by S. aureus was lower in patients than in controls. PNCs were more abundant in baseline samples from patients than in healthy controls and most bacterial isolates induced additional PNC formation and neutrophil activation.<br/><br>
<br/><br>
CONCLUSION/SIGNIFICANCE:<br/><br>
We have demonstrated for the first time that bacteria isolated from patients with Gram-positive bacteremia can induce platelet activation and aggregation, PNC formation, and neutrophil activation in the same infected host. This underlines the significance of these interactions during infection, which could be a target for future therapies in sepsis.}},
  author       = {{Johansson, Daniel and Shannon, Oonagh and Rasmussen, Magnus}},
  issn         = {{1932-6203}},
  language     = {{eng}},
  number       = {{11}},
  publisher    = {{Public Library of Science (PLoS)}},
  series       = {{PLoS ONE}},
  title        = {{Platelet and neutrophil responses to gram positive pathogens in patients with bacteremic infection.}},
  url          = {{https://lup.lub.lu.se/search/files/5239887/2375082.pdf}},
  doi          = {{10.1371/journal.pone.0026928}},
  volume       = {{6}},
  year         = {{2011}},
}