Abstract
To test our hypothesis that diesel exhaust particle (DEP)-induced oxidative stress and host antioxidant responses play a key role in the development of DEP-induced airway inflammatory diseases, C57BL/6 nuclear erythroid 2 P45-related factor 2 (Nrf2) knockout (Nrf2-/-) and wild-type mice were exposed to low-dose DEP for 7 h/day, 5 days/week, for 8 weeks. Nrf2-/- mice exposed to low-dose DEP showed significantly increased airway hyperresponsiveness and counts of lymphocytes and eosinophils, together with increased concentrations of IL-12 and IL-13, and thymus and activation-regulated chemokine (TARC), in BAL fluid than wild-type mice. In contrast, expression of antioxidant enzyme genes was significantly higher in wild-type mice than in Nrf2-/- mice. We have first demonstrated that disruption of Nrf2 enhances susceptibility to airway inflammatory responses induced by inhalation of low-dose DEP in mice. These results strongly suggest that DEP-induced oxidative stress and host antioxidant responses play some role in the development of DEP-induced airway inflammation.
Original language | English |
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Pages (from-to) | 366-373 |
Number of pages | 8 |
Journal | Clinical Immunology |
Volume | 128 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2008 Sep |
Externally published | Yes |
Keywords
- Airway hyperresponsiveness
- Cytokine
- Diesel exhaust particle
- Eosinophils
- Mouse model
- Nrf2
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology