Airborne particulate matter (PM_2.5) triggers cornea inflammation and pyroptosis via NLRP3 activation

Although studies have demonstrated that fine particulate matter (PM_2.5) induces ocular surface damage, PM2.5 exposure causes cornea toxicity is not entirely clear. The aim of this study is to investigate the role of the nod-like receptor family pyrin domain containing three (NLRP3) inflammasome-mediated pyroptosis in PM_2.5-related corneal toxicity. Human corneal epithelial cells (HCECs) were exposed to different concentrations of PM_2.5, and the cell viability, expressions of NLRP3 inflammasome mediated pyroptosis axis molecules and intracellular reactive oxygen species (ROS) formation were measured in HCECs. Animal experiments were undertaken to topically apply PM_2.5 suspension to mouse eyes for three months and the pyroptosis related molecules in the mouse corneas were measured. RESULTS: Our results showed a dose-dependent decrease of HCEC viability in the PM_2.5-treated cells. NLRP3 inflammasome-mediated pyroptosis axis (NLRP3, ASC, GSDMD, caspase-1, IL-1β, and IL-18) were activated in the PM_2.5-treated HCECs, accompanied by increased ROS formation. Further in vivo study confirmed the activation of this pathway in the mouse corneas exposed to PM_2.5. In conclusion, this study provids novel evidence that PM_2.5 induces corneal toxicity by triggering cell pyroptosis.