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

Saber AT, Lamson JS, Jacobsen NR, Ravn-Haren G, Hougaard KS, Nyendi AN, Wahlberg P, Madsen AM, Jackson P, Wallin H, Vogel U - PLoS ONE (2013)

Bottom Line: 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.Pulmonary acute phase response may constitute a direct link between particle inhalation and risk of cardiovascular disease.

View Article: PubMed Central - PubMed

Affiliation: The National Research Centre for the Working Environment, Copenhagen, Denmark. ats@nrcwe.dk

ABSTRACT

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.

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Dose-response effects in mice 1, 3 and 28 days after intratracheal instillation of MWCNT.A) Pulmonary Saa3 mRNA expression level; B) Hepatic Saa3 mRNA expression level, C) SAA3 concentration in BALF, and D) SAA3 protein in plasma. *, **, ***: Statistically significant compared to control mice at the 0.5, 0.01 and 0.001 level, respectively.
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pone-0069020-g002: Dose-response effects in mice 1, 3 and 28 days after intratracheal instillation of MWCNT.A) Pulmonary Saa3 mRNA expression level; B) Hepatic Saa3 mRNA expression level, C) SAA3 concentration in BALF, and D) SAA3 protein in plasma. *, **, ***: Statistically significant compared to control mice at the 0.5, 0.01 and 0.001 level, respectively.

Mentions: MWCNT induced the strongest acute phase response in lung, and mRNA expression of Saa3 was therefore also assessed in liver. MWCNT exposure did not change Saa3 expression in liver at any dose or time point (Figure 2B).


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

Saber AT, Lamson JS, Jacobsen NR, Ravn-Haren G, Hougaard KS, Nyendi AN, Wahlberg P, Madsen AM, Jackson P, Wallin H, Vogel U - PLoS ONE (2013)

Dose-response effects in mice 1, 3 and 28 days after intratracheal instillation of MWCNT.A) Pulmonary Saa3 mRNA expression level; B) Hepatic Saa3 mRNA expression level, C) SAA3 concentration in BALF, and D) SAA3 protein in plasma. *, **, ***: Statistically significant compared to control mice at the 0.5, 0.01 and 0.001 level, respectively.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3722244&req=5

pone-0069020-g002: Dose-response effects in mice 1, 3 and 28 days after intratracheal instillation of MWCNT.A) Pulmonary Saa3 mRNA expression level; B) Hepatic Saa3 mRNA expression level, C) SAA3 concentration in BALF, and D) SAA3 protein in plasma. *, **, ***: Statistically significant compared to control mice at the 0.5, 0.01 and 0.001 level, respectively.
Mentions: MWCNT induced the strongest acute phase response in lung, and mRNA expression of Saa3 was therefore also assessed in liver. MWCNT exposure did not change Saa3 expression in liver at any dose or time point (Figure 2B).

Bottom Line: 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.Pulmonary acute phase response may constitute a direct link between particle inhalation and risk of cardiovascular disease.

View Article: PubMed Central - PubMed

Affiliation: The National Research Centre for the Working Environment, Copenhagen, Denmark. ats@nrcwe.dk

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus