Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.

BACKGROUND: Particulate air pollution is associated with cardiovascular disease. Acute phase response is causally linked to cardiovascular disease. Here, we propose that particle-induced pulmonary acute phase response provides an underlying mechanism for particle-induced cardiovascular risk. METHODS...

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Main Authors: Anne Thoustrup Saber, Jacob Stuart Lamson, Nicklas Raun Jacobsen, Gitte Ravn-Haren, Karin Sørig Hougaard, Allen Njimeri Nyendi, Pia Wahlberg, Anne Mette Madsen, Petra Jackson, Håkan Wallin, Ulla Vogel
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3722244?pdf=render
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spelling doaj-1857cbcf06b64498a4b7c3641285f8ad2020-11-24T21:11:16ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0187e6902010.1371/journal.pone.0069020Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.Anne Thoustrup SaberJacob Stuart LamsonNicklas Raun JacobsenGitte Ravn-HarenKarin Sørig HougaardAllen Njimeri NyendiPia WahlbergAnne Mette MadsenPetra JacksonHåkan WallinUlla VogelBACKGROUND: Particulate air pollution is associated with cardiovascular disease. Acute phase response is causally linked to cardiovascular disease. Here, we propose that particle-induced pulmonary acute phase response provides an underlying mechanism for particle-induced cardiovascular risk. METHODS: We analysed the mRNA expression of Serum Amyloid A (Saa3) in lung tissue from female C57BL/6J mice exposed to different particles including nanomaterials (carbon black and titanium dioxide nanoparticles, multi- and single walled carbon nanotubes), diesel exhaust particles and airborne dust collected at a biofuel plant. Mice were exposed to single or multiple doses of particles by inhalation or intratracheal instillation and pulmonary mRNA expression of Saa3 was determined at different time points of up to 4 weeks after exposure. Also hepatic mRNA expression of Saa3, SAA3 protein levels in broncheoalveolar lavage fluid and in plasma and high density lipoprotein levels in plasma were determined in mice exposed to multiwalled carbon nanotubes. RESULTS: Pulmonary exposure to particles strongly increased Saa3 mRNA levels in lung tissue and elevated SAA3 protein levels in broncheoalveolar lavage fluid and plasma, whereas hepatic Saa3 levels were much less affected. Pulmonary Saa3 expression correlated with the number of neutrophils in BAL across different dosing regimens, doses and time points. CONCLUSIONS: Pulmonary acute phase response may constitute a direct link between particle inhalation and risk of cardiovascular disease. We propose that the particle-induced pulmonary acute phase response may predict risk for cardiovascular disease.http://europepmc.org/articles/PMC3722244?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Anne Thoustrup Saber
Jacob Stuart Lamson
Nicklas Raun Jacobsen
Gitte Ravn-Haren
Karin Sørig Hougaard
Allen Njimeri Nyendi
Pia Wahlberg
Anne Mette Madsen
Petra Jackson
Håkan Wallin
Ulla Vogel
spellingShingle Anne Thoustrup Saber
Jacob Stuart Lamson
Nicklas Raun Jacobsen
Gitte Ravn-Haren
Karin Sørig Hougaard
Allen Njimeri Nyendi
Pia Wahlberg
Anne Mette Madsen
Petra Jackson
Håkan Wallin
Ulla Vogel
Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.
PLoS ONE
author_facet Anne Thoustrup Saber
Jacob Stuart Lamson
Nicklas Raun Jacobsen
Gitte Ravn-Haren
Karin Sørig Hougaard
Allen Njimeri Nyendi
Pia Wahlberg
Anne Mette Madsen
Petra Jackson
Håkan Wallin
Ulla Vogel
author_sort Anne Thoustrup Saber
title Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.
title_short Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.
title_full Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.
title_fullStr Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.
title_full_unstemmed Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.
title_sort particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2013-01-01
description BACKGROUND: Particulate air pollution is associated with cardiovascular disease. Acute phase response is causally linked to cardiovascular disease. Here, we propose that particle-induced pulmonary acute phase response provides an underlying mechanism for particle-induced cardiovascular risk. METHODS: We analysed the mRNA expression of Serum Amyloid A (Saa3) in lung tissue from female C57BL/6J mice exposed to different particles including nanomaterials (carbon black and titanium dioxide nanoparticles, multi- and single walled carbon nanotubes), diesel exhaust particles and airborne dust collected at a biofuel plant. Mice were exposed to single or multiple doses of particles by inhalation or intratracheal instillation and pulmonary mRNA expression of Saa3 was determined at different time points of up to 4 weeks after exposure. Also hepatic mRNA expression of Saa3, SAA3 protein levels in broncheoalveolar lavage fluid and in plasma and high density lipoprotein levels in plasma were determined in mice exposed to multiwalled carbon nanotubes. RESULTS: Pulmonary exposure to particles strongly increased Saa3 mRNA levels in lung tissue and elevated SAA3 protein levels in broncheoalveolar lavage fluid and plasma, whereas hepatic Saa3 levels were much less affected. Pulmonary Saa3 expression correlated with the number of neutrophils in BAL across different dosing regimens, doses and time points. CONCLUSIONS: Pulmonary acute phase response may constitute a direct link between particle inhalation and risk of cardiovascular disease. We propose that the particle-induced pulmonary acute phase response may predict risk for cardiovascular disease.
url http://europepmc.org/articles/PMC3722244?pdf=render
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