TY - JOUR
T1 - Inhalation of carbon black nanoparticles aggravates pulmonary inflammation in mice
AU - Saputra, Devina
AU - Yoon, Jin ha
AU - Park, Hyunju
AU - Heo, Yongju
AU - Yang, Hyoseon
AU - Lee, Eun Ji
AU - Lee, Sangjin
AU - Song, Chang Woo
AU - Lee, Kyuhong
N1 - Publisher Copyright:
© 2014 The Korean Society of Toxicology. All rights reserved.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2014
Y1 - 2014
N2 - An increasing number of recent studies have focused on the impact of particulate matter on human health. As a model for atmospheric particulate inhalation, we investigated the effects of inhaled carbon black nanoparticles (CBNP) on mice with bleomycin-induced pulmonary fibrosis. The CNBPs were generated by a novel aerosolization process, and the mice were exposed to the aerosol for 4 hours. We found that CBNP inhalation exacerbated lung inflammation, as evidenced by histopathology analysis and by the expression levels of interleukin-6 protein, fibronectin, and interferon-γ mRNAs in lung tissues. Notably, fibronectin mRNA expression showed a statistically significant increase in expression after CBNP exposure. These data suggest that the concentration of CBNPs delivered (calculated to be 12.5 μg/m3) can aggravate lung inflammation in mice. Our results also suggest that the inhalation of ultrafine particles like PM 2.5 is an impactful environmental risk factor for humans, particularly in susceptible populations with predisposing lung conditions.
AB - An increasing number of recent studies have focused on the impact of particulate matter on human health. As a model for atmospheric particulate inhalation, we investigated the effects of inhaled carbon black nanoparticles (CBNP) on mice with bleomycin-induced pulmonary fibrosis. The CNBPs were generated by a novel aerosolization process, and the mice were exposed to the aerosol for 4 hours. We found that CBNP inhalation exacerbated lung inflammation, as evidenced by histopathology analysis and by the expression levels of interleukin-6 protein, fibronectin, and interferon-γ mRNAs in lung tissues. Notably, fibronectin mRNA expression showed a statistically significant increase in expression after CBNP exposure. These data suggest that the concentration of CBNPs delivered (calculated to be 12.5 μg/m3) can aggravate lung inflammation in mice. Our results also suggest that the inhalation of ultrafine particles like PM 2.5 is an impactful environmental risk factor for humans, particularly in susceptible populations with predisposing lung conditions.
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U2 - 10.5487/TR.2014.30.2.083
DO - 10.5487/TR.2014.30.2.083
M3 - Article
AN - SCOPUS:84921932106
VL - 30
SP - 83
EP - 90
JO - Toxicological Research
JF - Toxicological Research
SN - 1976-8257
IS - 2
ER -