TY - JOUR
T1 - Low dose carbon black nanoparticle exposure does not aggravate allergic airway inflammation in mice irrespective of the presence of surface polycyclic aromatic hydrocarbons
AU - Lindner, Karina
AU - Webering, Sina
AU - Stroebele, Michael
AU - Bockhorn, Henning
AU - Hansen, Tanja
AU - König, Peter
AU - Fehrenbach, Heinz
PY - 2018/4
Y1 - 2018/4
N2 - Exposure to exogenous noxae, such as particulate matter, can trigger acute aggravations of allergic asthma-a chronic inflammatory airway disease. We tested whether Carbon Black nanoparticles (CBNP) with or without surface polycyclic aromatic hydrocarbons (PAH) aggravate an established allergic airway inflammation in mice. In an ovalbumin mouse model, Printex®90 (P90), P90 coated with benzo[a]pyrene (P90-BaP) or 9-nitroanthracene (P90-9NA), or acetylene soot exhibiting a mixture of surface PAH (AS-PAH) was administered twice (70 µL, 100 µg/mL) during an established allergic airway inflammation. We analyzed the immune cell numbers and chemokine/cytokine profiles in bronchoalveolar lavages, the mRNA expressions of markers for PAH metabolism (Cyp1a1, 1b1), oxidative stress (HO-1, Gr, Gpx-3), inflammation (KC, Mcp-1, IL-6, IL-13, IL-17a), mucin synthesis (Muc5ac, Muc5b), the histology of mucus-producing goblet cells, ciliary beat frequency (CBF), and the particle transport speed. CBNP had a comparable primary particle size, hydrodynamic diameter, and η-potential, but differed in the specific surface area (P90 > P90-BaP = P90-9NA = AS-PAH) and surface chemistry. None of the CBNP tested increased any parameter related to inflammation. The unmodified P90, however, decreased the tracheal CBF, decreased the Muc5b in intrapulmonary airways, but increased the tracheal Muc5ac. Our results demonstrated that irrespective of the surface PAH, a low dose of CBNP does not acutely aggravate an established allergic airway inflammation in mice.
AB - Exposure to exogenous noxae, such as particulate matter, can trigger acute aggravations of allergic asthma-a chronic inflammatory airway disease. We tested whether Carbon Black nanoparticles (CBNP) with or without surface polycyclic aromatic hydrocarbons (PAH) aggravate an established allergic airway inflammation in mice. In an ovalbumin mouse model, Printex®90 (P90), P90 coated with benzo[a]pyrene (P90-BaP) or 9-nitroanthracene (P90-9NA), or acetylene soot exhibiting a mixture of surface PAH (AS-PAH) was administered twice (70 µL, 100 µg/mL) during an established allergic airway inflammation. We analyzed the immune cell numbers and chemokine/cytokine profiles in bronchoalveolar lavages, the mRNA expressions of markers for PAH metabolism (Cyp1a1, 1b1), oxidative stress (HO-1, Gr, Gpx-3), inflammation (KC, Mcp-1, IL-6, IL-13, IL-17a), mucin synthesis (Muc5ac, Muc5b), the histology of mucus-producing goblet cells, ciliary beat frequency (CBF), and the particle transport speed. CBNP had a comparable primary particle size, hydrodynamic diameter, and η-potential, but differed in the specific surface area (P90 > P90-BaP = P90-9NA = AS-PAH) and surface chemistry. None of the CBNP tested increased any parameter related to inflammation. The unmodified P90, however, decreased the tracheal CBF, decreased the Muc5b in intrapulmonary airways, but increased the tracheal Muc5ac. Our results demonstrated that irrespective of the surface PAH, a low dose of CBNP does not acutely aggravate an established allergic airway inflammation in mice.
UR - http://www.scopus.com/inward/record.url?scp=85045003058&partnerID=8YFLogxK
U2 - 10.3390/nano8040213
DO - 10.3390/nano8040213
M3 - Journal articles
AN - SCOPUS:85045003058
SN - 2079-4991
VL - 8
JO - Nanomaterials
JF - Nanomaterials
IS - 4
M1 - 213
ER -