Airborne particulate matter (PM2.5) triggers ocular hypertension through pyroptosis

Abstract

Background Particulate matter (PM) is strongly linked to human health and has detrimental effects on the eye. Studies have, however, focused on the ocular surface, with limited research on the impact of PM2.5 on intraocular pressure (IOP).Methods To investigate the impact of PM2.5 on IOP and the associated mechanism, C57BL/6 mouse eyes were topically exposed to a PM2.5 suspension for 3 months, and human trabecular meshwork (HTM) cells were subjected to various PM2.5 concentrations in vitro.Results The results revealed that the IOP increased gradually after PM2.5 exposure, and an upregulation of NLRP3 inflammasome, caspase-1, IL-1β, and GSDMD protein levels was observed in outflow tissues. PM2.5 exposure decreased HTM cell viability and affected contraction. Further, elevated ROS levels were observed as well as an activation of the NLRP3 inflammasome and downstream inflammatory factors caspase-1 and IL-1β. ROS scavenger or caspase-1 inhibitor treatment improved these PM2.5-induced changes.Conclusion This study provides novel evidence of the PM2.5-mediated development of ocular hypertension, which occurs as a result of increased oxidative stress and the subsequent induction of pyroptosis in trabecular meshwork cells.