Lung exposure to nanoparticles modulates an asthmatic response in a mouse model of asthma
Hussain S, Vanoirbeek JA, Luyts K, De Vooght V, Verbeken E, Thomassen LC, Martens JA, Dinsdale D, Boland S, Marano F, Nemery B, Hoet PH.
Univ. Paris Diderot, Paris France.
Eur Respir J. 2010 Jun 7.
Abstract
The aim of this study was to investigate the modulation of an asthmatic response by titanium dioxide (TiO2) or gold (Au) nanoparticles (NPs) in a murine model of diisocyanate-induced asthma. On days 1 and 8, BALB/c mice received 0.3% toluene diisocyanate (TDI) or the vehicle acetone-olive oil (AOO) on the dorsum of both ears (20 mul). On day 14, the mice were oropharyngeally dosed with 40 mul of a NP suspension (0.4 mg.mL(-1) approximately 0.8 mg.kg(-1) TiO2 or Au). One day later (day 15), the mice received an oropharyngeal challenge with 0.01%TDI (20 mul). On day 16, airway hyperreactivity (AHR), bronchoalveolar lavage (BAL) cell and cytokine analysis, lung histology and total serum IgE were assessed. NP exposure in sensitized mice led to a 2-fold (TiO2) and 3-fold (AU) increase in AHR, and a 3-fold or 5-fold increase in BAL total cell counts, mainly comprising neutrophils and macrophages. The NPs taken up by BAL macrophages were identified by energy dispersive X-ray spectroscopy (EDX). Histological analysis revealed increased oedema, epithelial damage and inflammation. In conclusion, these results show that a low, intrapulmonary, dose TiO2 or Au NPs can aggravate pulmonary inflammation and AHR in a mouse model of diisocyanate-induced asthma.
PMID: 20530043 [PubMed - as supplied by publisher]
Hussain S, Vanoirbeek JA, Luyts K, De Vooght V, Verbeken E, Thomassen LC, Martens JA, Dinsdale D, Boland S, Marano F, Nemery B, Hoet PH.
Univ. Paris Diderot, Paris France.
Eur Respir J. 2010 Jun 7.
Abstract
The aim of this study was to investigate the modulation of an asthmatic response by titanium dioxide (TiO2) or gold (Au) nanoparticles (NPs) in a murine model of diisocyanate-induced asthma. On days 1 and 8, BALB/c mice received 0.3% toluene diisocyanate (TDI) or the vehicle acetone-olive oil (AOO) on the dorsum of both ears (20 mul). On day 14, the mice were oropharyngeally dosed with 40 mul of a NP suspension (0.4 mg.mL(-1) approximately 0.8 mg.kg(-1) TiO2 or Au). One day later (day 15), the mice received an oropharyngeal challenge with 0.01%TDI (20 mul). On day 16, airway hyperreactivity (AHR), bronchoalveolar lavage (BAL) cell and cytokine analysis, lung histology and total serum IgE were assessed. NP exposure in sensitized mice led to a 2-fold (TiO2) and 3-fold (AU) increase in AHR, and a 3-fold or 5-fold increase in BAL total cell counts, mainly comprising neutrophils and macrophages. The NPs taken up by BAL macrophages were identified by energy dispersive X-ray spectroscopy (EDX). Histological analysis revealed increased oedema, epithelial damage and inflammation. In conclusion, these results show that a low, intrapulmonary, dose TiO2 or Au NPs can aggravate pulmonary inflammation and AHR in a mouse model of diisocyanate-induced asthma.
PMID: 20530043 [PubMed - as supplied by publisher]
