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Neutrophil Activation Status in Stable Coronary Artery Disease

BACKGROUND: During the last years, neutrophils have emerged as important players in atherogenesis. They are highly activated in peripheral blood of patients with unstable angina. Moreover, a primed state of circulating neutrophils has been proposed in patients with stable angina. Our aim was to inve...

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Autores principales: Särndahl, Eva, Bergström, Ida, Brodin, Veronika Patcha, Nijm, Johnny, Setterud, Helen Lundqvist, Jonasson, Lena
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2020438/
https://www.ncbi.nlm.nih.gov/pubmed/17957240
http://dx.doi.org/10.1371/journal.pone.0001056
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author Särndahl, Eva
Bergström, Ida
Brodin, Veronika Patcha
Nijm, Johnny
Setterud, Helen Lundqvist
Jonasson, Lena
author_facet Särndahl, Eva
Bergström, Ida
Brodin, Veronika Patcha
Nijm, Johnny
Setterud, Helen Lundqvist
Jonasson, Lena
author_sort Särndahl, Eva
collection PubMed
description BACKGROUND: During the last years, neutrophils have emerged as important players in atherogenesis. They are highly activated in peripheral blood of patients with unstable angina. Moreover, a primed state of circulating neutrophils has been proposed in patients with stable angina. Our aim was to investigate the neutrophil activation status in patients with stable coronary artery disease (CAD) at conventional drug treatment. METHODOLOGY AND PRINCIPAL FINDINGS: Thirty patients with stable CAD and 30 healthy controls were included using a paired design. The neutrophil expression of CD18 and high-affinity state of CD11b was analysed by flow cytometry before and after stimulation with chemoattractants. Also, the production of reactive oxygen species (ROS) was determined by chemiluminescence. During basal conditions, the neutrophil expression of CD18 or high-affinity state of CD11b did not differ between patients and controls. Chemoattractants (Interleukin-8 and Leukotriene B(4)) did not increase either the expression or the amount of high-affinity CD11b/CD18-integrins in CAD patients compared to controls, and had no effect on the production of ROS. On the other hand, the ROS production in response to C3bi-opsonised yeast particles and the neutrophils' inherent capacity to produce ROS were both significantly decreased in patients. CONCLUSION/SIGNIFICANCE: We could not find any evidence that neutrophils in patients with stable CAD were primed, i.e. more prone to activation, compared to cells from healthy controls. According to our data, the circulating neutrophils in CAD patients rather showed an impaired activation status. It remains to be elucidated whether the neutrophil dysfunction in CAD is mainly a marker of chronic disease, an atherogenic factor or a consequence of the drug treatment.
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spelling pubmed-20204382007-10-24 Neutrophil Activation Status in Stable Coronary Artery Disease Särndahl, Eva Bergström, Ida Brodin, Veronika Patcha Nijm, Johnny Setterud, Helen Lundqvist Jonasson, Lena PLoS One Research Article BACKGROUND: During the last years, neutrophils have emerged as important players in atherogenesis. They are highly activated in peripheral blood of patients with unstable angina. Moreover, a primed state of circulating neutrophils has been proposed in patients with stable angina. Our aim was to investigate the neutrophil activation status in patients with stable coronary artery disease (CAD) at conventional drug treatment. METHODOLOGY AND PRINCIPAL FINDINGS: Thirty patients with stable CAD and 30 healthy controls were included using a paired design. The neutrophil expression of CD18 and high-affinity state of CD11b was analysed by flow cytometry before and after stimulation with chemoattractants. Also, the production of reactive oxygen species (ROS) was determined by chemiluminescence. During basal conditions, the neutrophil expression of CD18 or high-affinity state of CD11b did not differ between patients and controls. Chemoattractants (Interleukin-8 and Leukotriene B(4)) did not increase either the expression or the amount of high-affinity CD11b/CD18-integrins in CAD patients compared to controls, and had no effect on the production of ROS. On the other hand, the ROS production in response to C3bi-opsonised yeast particles and the neutrophils' inherent capacity to produce ROS were both significantly decreased in patients. CONCLUSION/SIGNIFICANCE: We could not find any evidence that neutrophils in patients with stable CAD were primed, i.e. more prone to activation, compared to cells from healthy controls. According to our data, the circulating neutrophils in CAD patients rather showed an impaired activation status. It remains to be elucidated whether the neutrophil dysfunction in CAD is mainly a marker of chronic disease, an atherogenic factor or a consequence of the drug treatment. Public Library of Science 2007-10-24 /pmc/articles/PMC2020438/ /pubmed/17957240 http://dx.doi.org/10.1371/journal.pone.0001056 Text en Särndahl et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Särndahl, Eva
Bergström, Ida
Brodin, Veronika Patcha
Nijm, Johnny
Setterud, Helen Lundqvist
Jonasson, Lena
Neutrophil Activation Status in Stable Coronary Artery Disease
title Neutrophil Activation Status in Stable Coronary Artery Disease
title_full Neutrophil Activation Status in Stable Coronary Artery Disease
title_fullStr Neutrophil Activation Status in Stable Coronary Artery Disease
title_full_unstemmed Neutrophil Activation Status in Stable Coronary Artery Disease
title_short Neutrophil Activation Status in Stable Coronary Artery Disease
title_sort neutrophil activation status in stable coronary artery disease
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2020438/
https://www.ncbi.nlm.nih.gov/pubmed/17957240
http://dx.doi.org/10.1371/journal.pone.0001056
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