Y Miyabara1, T Ichinose, H Takano, M Sagai. 1. Research Team for Health Effects of Air Pollutants, National Institute for Environmental Studies, Ibaraki, Japan. miyabara@nies.go.jp
Abstract
BACKGROUND: Repeated intratracheal instillation of diesel exhaust particles and ovalbumin-induced airway hyperresponsiveness and airway inflammation in mice. However, the effects of daily inhalation of diesel exhaust may differ from the effects of direct instillation. METHODS: Therefore, mice were exposed to diesel exhaust by inhalation 12 h per day for 3 months. Before the diesel exhaust exposure, ovalbumin was injected intraperitoneally as a sensitization. After 3 weeks of diesel exhaust exposure, these mice were challenged with ovalbumin every 3 week thereafter. RESULTS: Diesel exhaust exposure with antigen challenge induced airway hyperresponsiveness and airway inflammation which was characterized by increased numbers of eosinophils and mast cells in lung tissue. The recruitment of inflammatory cells was accompanied by an increment in goblet cells on bronchial epithelium. Diesel exhaust exposure alone also enhanced airway hyperresponsiveness, but did not induce eosinophilic infiltration and/or an increment in goblet cells. CONCLUSION: Diesel exhaust inhalation enhanced airway hyperresponsiveness and airway inflammation caused by ovalbumin sensitization in mice.
BACKGROUND: Repeated intratracheal instillation of diesel exhaust particles and ovalbumin-induced airway hyperresponsiveness and airway inflammation in mice. However, the effects of daily inhalation of diesel exhaust may differ from the effects of direct instillation. METHODS: Therefore, mice were exposed to diesel exhaust by inhalation 12 h per day for 3 months. Before the diesel exhaust exposure, ovalbumin was injected intraperitoneally as a sensitization. After 3 weeks of diesel exhaust exposure, these mice were challenged with ovalbumin every 3 week thereafter. RESULTS: Diesel exhaust exposure with antigen challenge induced airway hyperresponsiveness and airway inflammation which was characterized by increased numbers of eosinophils and mast cells in lung tissue. The recruitment of inflammatory cells was accompanied by an increment in goblet cells on bronchial epithelium. Diesel exhaust exposure alone also enhanced airway hyperresponsiveness, but did not induce eosinophilic infiltration and/or an increment in goblet cells. CONCLUSION: Diesel exhaust inhalation enhanced airway hyperresponsiveness and airway inflammation caused by ovalbumin sensitization in mice.
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