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Article

Nrf2 Regulates the Risk of a Diesel Exhaust Inhalation-Induced Immune Response during Bleomycin Lung Injury and Fibrosis in Mice

1
Department of Hygiene and Public Health, Nippon Medical School, Tokyo 113-0031, Japan
2
The Center for Environmental Health Science for the Next Generation, Research Institute for Science and Technology, Tokyo University of Science, Noda 278-8510, Japan
3
Department of Pulmonary Medicine/Infection and Oncology, Nippon Medical School, Tokyo 113-8602, Japan
4
Department of Biochemistry, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan
*
Author to whom correspondence should be addressed.
Academic Editors: Paul R. Reynolds and Benjamin T. Bikman
Int. J. Mol. Sci. 2017, 18(3), 649; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18030649
Received: 28 January 2017 / Revised: 3 March 2017 / Accepted: 9 March 2017 / Published: 17 March 2017
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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. View Full-Text
Keywords: diesel exhaust; bleomycin; lung injury and fibrosis; Nrf2; oxidative stress/antioxidative stress diesel exhaust; bleomycin; lung injury and fibrosis; Nrf2; oxidative stress/antioxidative stress
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MDPI and ACS Style

Li, Y.-J.; Shimizu, T.; Shinkai, Y.; Hirata, Y.; Inagaki, H.; Takeda, K.; Azuma, A.; Yamamoto, M.; Kawada, T. Nrf2 Regulates the Risk of a Diesel Exhaust Inhalation-Induced Immune Response during Bleomycin Lung Injury and Fibrosis in Mice. Int. J. Mol. Sci. 2017, 18, 649. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18030649

AMA Style

Li Y-J, Shimizu T, Shinkai Y, Hirata Y, Inagaki H, Takeda K, Azuma A, Yamamoto M, Kawada T. Nrf2 Regulates the Risk of a Diesel Exhaust Inhalation-Induced Immune Response during Bleomycin Lung Injury and Fibrosis in Mice. International Journal of Molecular Sciences. 2017; 18(3):649. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18030649

Chicago/Turabian Style

Li, Ying-Ji, Takako Shimizu, Yusuke Shinkai, Yukiyo Hirata, Hirofumi Inagaki, Ken Takeda, Arata Azuma, Masayuki Yamamoto, and Tomoyuki Kawada. 2017. "Nrf2 Regulates the Risk of a Diesel Exhaust Inhalation-Induced Immune Response during Bleomycin Lung Injury and Fibrosis in Mice" International Journal of Molecular Sciences 18, no. 3: 649. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18030649

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