Nrf2 regulates the risk of a diesel exhaust inhalation-induced immune response during bleomycin lung injury and fibrosis in mice

Ying Ji Li, Takako Shimizu, Yusuke Shinkai, Yukiyo Hirata, Hirofumi Inagaki, Ken Takeda, Arata Azuma, Masayuki Yamamoto, Tomoyuki Kawada

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)

Abstract

The present study investigated the effects of diesel exhaust (DE) on an experimental model of bleomycin (BLM)-induced lung injury and fibrosis in mice. BLM was intravenously administered to both Nrf2+/+ and Nrf2−/− C57BL/6J mice on day 0. The mice were exposed to DE for 56 days from 28 days before the BLM injection to 28 days after the BLM injection. Inhalation of DE induced significant inhibition of airway clearance function and the proinflammatory cytokine secretion in macrophages, an increase in neutrophils, and severe lung inflammatory injury, which were greater in Nrf2−/− mice than in Nrf2+/+ mice. In contrast, inhalation of DE was observed to induce a greater increase of hydroxyproline content in the lung tissues and significantly higher pulmonary antioxidant enzyme mRNA expression in the Nrf2+/+ mice than in Nrf2−/− mice. DE is an important risk factor, and Nrf2 regulates the risk of a DE inhalation induced immune response during BLM lung injury and fibrosis in mice.

Original languageEnglish
Article number649
JournalInternational journal of molecular sciences
Volume18
Issue number3
DOIs
Publication statusPublished - 2017 Mar 17

Keywords

  • Bleomycin
  • Diesel exhaust
  • Lung injury and fibrosis
  • Nrf2
  • Oxidative stress/antioxidative stress

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

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