Nrf2 modulated the restriction of lung function via impairment of intrinsic autophagy upon real-ambient PM2.5 exposure.

Compelling studies approve that fine particle matter (PM2.5) exposure was associated with high risk of respiratory disorders. However, the available data assessing the detailed influence of PM2.5 on lung was limited. To overcome the difficulty of inhalational PM2.5 exposure, the real-ambient PM2.5 exposure system was constructed. The mice were exposed to filtered air (FA) or real-ambient PM2.5 (PM2.5), and the adverse effect on lung was determined. Nuclear factor E2-related factor 2 (Nrf2) as a transcription factor, was reported to affect autophagy. Autophagy was proposed as a two-edge sword in respiratory disorders. Here, our data presented that PM2.5 exposure dramatically reduced the lung function of WT mice rather than Nrf2-/- mice. Consistently, thickened alveolar walls was observed in WT mice in PM2.5 exposure group, whereas the histological phenotype of Nrf2-/- mice exhibited no obvious alteration. Furthermore, PM2.5 exposure triggered low-grade production of inflammatory profile in WT and Nrf2-/- mice. Moreover, the protein levels of p62, Beclin1 and LC3B of WT mice rather than Nrf2-/- mice were also altered in PM2.5 exposure group. Taken together, the present study applied the real-ambient exposure system, revealed the adverse effect of air pollution on lung, and proposed the underlying mechanism.