| First Author | Li YJ | Year | 2020 |
| Journal | Biomedicines | Volume | 8 |
| Issue | 10 | PubMed ID | 33096811 |
| Mgi Jnum | J:303102 | Mgi Id | MGI:6511360 |
| Doi | 10.3390/biomedicines8100443 | Citation | Li YJ, et al. (2020) Nrf2 Lowers the Risk of Lung Injury via Modulating the Airway Innate Immune Response Induced by Diesel Exhaust in Mice. Biomedicines 8(10) |
| abstractText | In the present study, we investigated the role of Nrf2 in airway immune responses induced by diesel exhaust (DE) inhalation in mice. C57BL/6J Nrf2(+/+) and Nrf2(-/-) mice were exposed to DE or clean air for 8 h/day and 6 days/week for 4 weeks. After DE exposure, the number of neutrophils and macrophage inflammatory protein (MIP)-2 level in bronchoalveolar lavage fluid (BALF) and interleukin (IL)-17 level in the lung tissue increased in Nrf2(-/-) mice compared with Nrf2(+/+) mice; however, the lack of an increase in the level of tumor necrosis factor (TNF)-alpha in the lung tissue in Nrf2(+/+) mice and mild suppression of the level of TNF-alpha in Nrf2(-/-) mice were observed; the level of granulocyte macrophage colony-stimulating factor (GM-CSF) in the lung tissue decreased in Nrf2(-/-) mice than in Nrf2(+/+) mice; the number of DE particle-laden alveolar macrophages in BALF were larger in Nrf2(-/-) mice than in Nrf2(+/+) mice. The results of electron microscope observations showed alveolar type II cell injury and degeneration of the lamellar body after DE exposure in Nrf2(-/-) mice. Antioxidant enzyme NAD(P)H quinone dehydrogenase (NQO)1 mRNA expression level was higher in Nrf2(+/+) mice than in Nrf2(-/-) mice after DE exposure. Our results suggested that Nrf2 reduces the risk of pulmonary disease via modulating the airway innate immune response caused by DE in mice. |
