PM2.5 induces autophagy-mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

Air pollution can highly impact the respiratory system in healthy individuals. Studies have indicated that particles with an aerodynamic diameter of <= 2.5 mu m (PM2.5) can be considered to be harmful for lung alveoli and bronchial epithelium cells. PM2.5 can be directly inhaled and can deeply penetrate into the lung alveoli, causing lung dysfunction. However, the toxicological mechanism mediated by PM2.5 for respiratory disease has still not been clearly determined. The purpose of the current study was to investigate the effects of PM2.5 on mouse bronchial epithelium cells (MBECs) and explored the possible mechanism mediated by PM2.5 in MBECs. The results of the current study indicated that PM2.5 markedly decreased lung function, including total lung capacity, residual volume, vital capacity and airway resistance in experimental mice. The results demonstrated that PM2.5 markedly induced inflammatory responses, oxidative injury and MBEC apoptosis. PM2.5 increased interleukin (IL)-1 beta and IL-6 expression, and reactive oxygen species production in MBECs. Furthermore, PM2.5 specifically induced PI3K, AKT and mTOR expression in MBECs. Disruption of PI3K/AKT/mTOR signaling was also indicated to effectively inhibit apoptosis of MBECs. In conclusion, the results of the current study systematically demonstrated the role of apoptosis-mediated MBEC apoptosis in PM2.5-treated mice, and provides a potential strategy for preclinical intervention in patients with PM2.5-induced lung diseases.

Automated summary

The study found that PM2.5 significantly decreased lung function in mice, induced inflammatory responses, oxidative injury, and bronchial epithelium cell apoptosis. PM2.5 also increased IL-1β, IL-6 expression, reactive oxygen species production, and induced PI3K, AKT, and mTOR expression in MBECs.