The dynamics of platelet activation during the progression of streptococcal sepsis
(2016) In PLoS ONE 11(9).- Abstract
Platelets contribute to inflammation however, the role of platelet activation during the pathophysiological response to invasive bacterial infection and sepsis is not clear. Herein, we have investigated platelet activation in a mouse model of invasive Streptococcus pyogenes infection at 5,12, and 18 hours post infection and correlated this to parameters of infection. The platelet population in ex-vivo blood samples showed no increased integrin activation or surface presentation of CD62P, however platelet-neutrophil complex formation and plasma levels of CD62P were increased during bacterial dissemination and the progression of sepsis, indicating that platelet activation had occurred in vivo. Platelet-neutrophil complex formation was the... (More)
Platelets contribute to inflammation however, the role of platelet activation during the pathophysiological response to invasive bacterial infection and sepsis is not clear. Herein, we have investigated platelet activation in a mouse model of invasive Streptococcus pyogenes infection at 5,12, and 18 hours post infection and correlated this to parameters of infection. The platelet population in ex-vivo blood samples showed no increased integrin activation or surface presentation of CD62P, however platelet-neutrophil complex formation and plasma levels of CD62P were increased during bacterial dissemination and the progression of sepsis, indicating that platelet activation had occurred in vivo. Platelet-neutrophil complex formation was the most discriminatory marker of platelet activation. Platelet-neutrophil complexes were increased above baseline levels during early sepsis but decreased to significantly lower levels than baseline during late sepsis. The removal of these complexes from the circulation coincided with a significant increase in organ damage and the accumulation of platelets in the liver sinusoids, suggesting that platelet activation in the circulation precedes accumulation of platelets in damaged organs. The results demonstrate that monitoring platelet activation using complementary methods may provide prognostic information during the pathogenesis of invasive S. pyogenes infection.
(Less)
- author
- Hurley, Sinead M. LU ; Lutay, Nataliya ; Holmqvist, Bo and Shannon, Oonagh LU
- organization
- publishing date
- 2016-09-01
- type
- Contribution to journal
- publication status
- published
- subject
- in
- PLoS ONE
- volume
- 11
- issue
- 9
- article number
- e0163531
- publisher
- Public Library of Science (PLoS)
- external identifiers
-
- scopus:84992175090
- pmid:27656898
- wos:000383893200139
- ISSN
- 1932-6203
- DOI
- 10.1371/journal.pone.0163531
- language
- English
- LU publication?
- yes
- id
- 2541b9b6-e3ba-471f-b2d7-643860c24870
- date added to LUP
- 2016-11-04 09:16:13
- date last changed
- 2024-04-05 09:27:51
@article{2541b9b6-e3ba-471f-b2d7-643860c24870,
abstract = {{<p>Platelets contribute to inflammation however, the role of platelet activation during the pathophysiological response to invasive bacterial infection and sepsis is not clear. Herein, we have investigated platelet activation in a mouse model of invasive Streptococcus pyogenes infection at 5,12, and 18 hours post infection and correlated this to parameters of infection. The platelet population in ex-vivo blood samples showed no increased integrin activation or surface presentation of CD62P, however platelet-neutrophil complex formation and plasma levels of CD62P were increased during bacterial dissemination and the progression of sepsis, indicating that platelet activation had occurred in vivo. Platelet-neutrophil complex formation was the most discriminatory marker of platelet activation. Platelet-neutrophil complexes were increased above baseline levels during early sepsis but decreased to significantly lower levels than baseline during late sepsis. The removal of these complexes from the circulation coincided with a significant increase in organ damage and the accumulation of platelets in the liver sinusoids, suggesting that platelet activation in the circulation precedes accumulation of platelets in damaged organs. The results demonstrate that monitoring platelet activation using complementary methods may provide prognostic information during the pathogenesis of invasive S. pyogenes infection.</p>}},
author = {{Hurley, Sinead M. and Lutay, Nataliya and Holmqvist, Bo and Shannon, Oonagh}},
issn = {{1932-6203}},
language = {{eng}},
month = {{09}},
number = {{9}},
publisher = {{Public Library of Science (PLoS)}},
series = {{PLoS ONE}},
title = {{The dynamics of platelet activation during the progression of streptococcal sepsis}},
url = {{http://dx.doi.org/10.1371/journal.pone.0163531}},
doi = {{10.1371/journal.pone.0163531}},
volume = {{11}},
year = {{2016}},
}