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Anti-platelet drugs attenuate the expansion of circulating CD14(high)CD16(+) monocytes under pro-inflammatory conditions

AIMS: Levels of circulating CD14(high)CD16(+) monocytes increase in atherosclerotic patients and are predictive of future cardiovascular events. Platelet activation has been identified as a crucial determinant in the acquisition of a CD16(+) phenotype by classical CD14(high)CD16(−) cells. We tested...

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Autores principales: Layne, Kerry, Di Giosia, Paolo, Ferro, Albert, Passacquale, Gabriella
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4909161/
https://www.ncbi.nlm.nih.gov/pubmed/27118470
http://dx.doi.org/10.1093/cvr/cvw089
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author Layne, Kerry
Di Giosia, Paolo
Ferro, Albert
Passacquale, Gabriella
author_facet Layne, Kerry
Di Giosia, Paolo
Ferro, Albert
Passacquale, Gabriella
author_sort Layne, Kerry
collection PubMed
description AIMS: Levels of circulating CD14(high)CD16(+) monocytes increase in atherosclerotic patients and are predictive of future cardiovascular events. Platelet activation has been identified as a crucial determinant in the acquisition of a CD16(+) phenotype by classical CD14(high)CD16(−) cells. We tested the hypothesis that anti-platelet drugs modulate the phenotype of circulating monocytes. METHODS AND RESULTS: Sixty healthy subjects undergoing influenza immunization were randomly assigned to either no treatment or anti-platelet therapy, namely aspirin 300 mg or 75 mg daily, or clopidogrel (300 mg loading dose followed by 75 mg), for 48 h post-immunization (n = 15/group). Monocyte subsets, high-sensitivity C-reactive protein, pro-inflammatory cytokines, and P-selectin were measured at baseline and post-immunization. The CD14(high)CD16(+) monocyte cell count rose by 67.3% [interquartile range (IQR): 35.7/169.2; P = 0.0002 vs. baseline] in untreated participants. All anti-platelet regimes counteracted expansion of this monocytic subpopulation. Although no statistical differences were noted among the three treatments, aspirin 300 mg was the most efficacious compared with the untreated group (−12.5% change from baseline; IQR: −28.7/18.31; P = 0.001 vs. untreated). Similarly, the rise in P-selectin (17%; IQR: −5.0/39.7; P = 0.03 vs. baseline) observed in untreated participants was abolished by all treatments, with aspirin 300 mg exerting the strongest effect (−30.7%; IQR: −58.4/−0.03; P = 0.007 vs. untreated). Changes in P-selectin levels directly correlated with changes in CD14(high)CD16(+) cell count (r = 0.5; P = 0.0002). There was a similar increase among groups in high-sensitivity C-reactive protein (P < 0.03 vs. baseline levels). CONCLUSIONS: Anti-platelet drugs exert an immunomodulatory action by counteracting CD14(high)CD16(+) monocyte increase under pro-inflammatory conditions, with this effect being dependent on the amplitude of P-selectin reduction.
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spelling pubmed-49091612016-06-17 Anti-platelet drugs attenuate the expansion of circulating CD14(high)CD16(+) monocytes under pro-inflammatory conditions Layne, Kerry Di Giosia, Paolo Ferro, Albert Passacquale, Gabriella Cardiovasc Res Original Articles AIMS: Levels of circulating CD14(high)CD16(+) monocytes increase in atherosclerotic patients and are predictive of future cardiovascular events. Platelet activation has been identified as a crucial determinant in the acquisition of a CD16(+) phenotype by classical CD14(high)CD16(−) cells. We tested the hypothesis that anti-platelet drugs modulate the phenotype of circulating monocytes. METHODS AND RESULTS: Sixty healthy subjects undergoing influenza immunization were randomly assigned to either no treatment or anti-platelet therapy, namely aspirin 300 mg or 75 mg daily, or clopidogrel (300 mg loading dose followed by 75 mg), for 48 h post-immunization (n = 15/group). Monocyte subsets, high-sensitivity C-reactive protein, pro-inflammatory cytokines, and P-selectin were measured at baseline and post-immunization. The CD14(high)CD16(+) monocyte cell count rose by 67.3% [interquartile range (IQR): 35.7/169.2; P = 0.0002 vs. baseline] in untreated participants. All anti-platelet regimes counteracted expansion of this monocytic subpopulation. Although no statistical differences were noted among the three treatments, aspirin 300 mg was the most efficacious compared with the untreated group (−12.5% change from baseline; IQR: −28.7/18.31; P = 0.001 vs. untreated). Similarly, the rise in P-selectin (17%; IQR: −5.0/39.7; P = 0.03 vs. baseline) observed in untreated participants was abolished by all treatments, with aspirin 300 mg exerting the strongest effect (−30.7%; IQR: −58.4/−0.03; P = 0.007 vs. untreated). Changes in P-selectin levels directly correlated with changes in CD14(high)CD16(+) cell count (r = 0.5; P = 0.0002). There was a similar increase among groups in high-sensitivity C-reactive protein (P < 0.03 vs. baseline levels). CONCLUSIONS: Anti-platelet drugs exert an immunomodulatory action by counteracting CD14(high)CD16(+) monocyte increase under pro-inflammatory conditions, with this effect being dependent on the amplitude of P-selectin reduction. Oxford University Press 2016-07-01 2016-04-26 /pmc/articles/PMC4909161/ /pubmed/27118470 http://dx.doi.org/10.1093/cvr/cvw089 Text en © The Author 2016. Published by Oxford University Press on behalf of the European Society of Cardiology. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Layne, Kerry
Di Giosia, Paolo
Ferro, Albert
Passacquale, Gabriella
Anti-platelet drugs attenuate the expansion of circulating CD14(high)CD16(+) monocytes under pro-inflammatory conditions
title Anti-platelet drugs attenuate the expansion of circulating CD14(high)CD16(+) monocytes under pro-inflammatory conditions
title_full Anti-platelet drugs attenuate the expansion of circulating CD14(high)CD16(+) monocytes under pro-inflammatory conditions
title_fullStr Anti-platelet drugs attenuate the expansion of circulating CD14(high)CD16(+) monocytes under pro-inflammatory conditions
title_full_unstemmed Anti-platelet drugs attenuate the expansion of circulating CD14(high)CD16(+) monocytes under pro-inflammatory conditions
title_short Anti-platelet drugs attenuate the expansion of circulating CD14(high)CD16(+) monocytes under pro-inflammatory conditions
title_sort anti-platelet drugs attenuate the expansion of circulating cd14(high)cd16(+) monocytes under pro-inflammatory conditions
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4909161/
https://www.ncbi.nlm.nih.gov/pubmed/27118470
http://dx.doi.org/10.1093/cvr/cvw089
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