Disruption of Nrf2 enhances susceptibility to airway inflammatory responses induced by low-dose diesel exhaust particles in mice

Ying Ji Li, Hajime Takizawa, Arata Azuma, Tadashi Kohyama, Yasuhiro Yamauchi, Satoru Takahashi, Masayuki Yamamoto, Tomoyuki Kawada, Shoji Kudoh, Isamu Sugawara

研究成果: Article査読

62 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)366-373
ページ数8
ジャーナルClinical Immunology
128
3
DOI
出版ステータスPublished - 2008 9月
外部発表はい

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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