Pyroptosis participates in PM_2.5-induced air-blood barrier dysfunction

Epidemiological studies have shown that particulate matters with diameter less than 2.5 μm (PM_2.5) play an important role in inducing and promoting respiratory diseases, but its underlying mechanism remains to be explored. The air-blood barrier, also known as the alveolar-capillary barrier, is the key element of the lung, working as the site of oxygen and carbon dioxide exchange between pulmonary vasculatures. In this study, a mouse PM_2.5 exposure model was established, which leads to an induced lung injury and air-blood barrier disruption. Oxidative stress and pyroptosis were observed in this process. After reducing the oxidative stress by N-acetyl-L-cysteine (NAC) treatment, the air-blood barrier function was improved and the effect of PM_2.5 was alleviated. The level of pyroptosis and related pathway were also effectively relieved. These results indicate that acute PM_2.5 exposure can cause lung injury and the alveolar-capillary barrier disruption by inducing reactive oxygen species (ROS) with the participation of pyroptosis pathway.