PM2.5 induced lung injury through upregulating ROS-dependent NLRP3 Inflammasome-Mediated

The main cause of air pollution is PM2.5, which directly causes lung injury through respiration. Oxidative stress and inflammation are considered to be the key mechanism of cell damage. Pyroptosis is a process of the programmed death of inflammatory cells and as a dangerous endogenous signal, it is widely involved in different inflammatory diseases. However, few studies have been conducted on PM2.5 exposure and cell pyroptosis. In this study, we aimed to investigate the effect of PM2.5 on apoptosis, pyroptosis and cell cycle arrest regulated by reactive oxygen species production. Balb/c mice were exposed to PM2.5 dynamically and verified by the RAW264.7 cells in vitro. The results showed the activation of NF-kappa B and NLRP3 inflammasome and the release of IL-1 beta and reactive oxygen species were caused by exposure to PM2.5. The maturation of IL-1 beta relied on Caspase-1, and the active Caspase-1 was related to cell pyroptosis. Oxidative stress, inflammation, apoptosis and pyroptosis all affected the cell cycle. This study describes a potentially important mechanism of PM2.5-induced lung damage that PM2.5 promotes lung injury via upregulating ROS-NLRP3-mediated the RAW264.7 cells pyroptosis.

Automated summary

This study reveals that exposure to PM2.5 can activate NF-κB and NLRP3 inflammasome, leading to the release of IL-1β and reactive oxygen species, which in turn trigger cell pyroptosis and disrupt the cell cycle. This may be an important mechanism of PM2.5-induced lung damage.