Fine Particulate Matter (PM2.5) upregulates expression of Inflammasome NLRP1 via ROS/NF-κB signaling in HaCaT Cells

Skin, as the major organ of a human body, is constantly exposed to PM2.5 stimulation, which may exert specific toxic influences on the physiology of skin. This study aims to investigate the effect of PM2.5 on the formation of inflammasomes in skin cells and to explore the potential mechanism linking PM2.5 and skin inflammation. Changes in mRNA and protein levels of inflammasome-related genes were detected by real-time PCR and western blot in human immortalized epidermal cells (HaCaT) treated with PM2.5 at multiple concentrations for 24 hours. The expression of NLRP1 was increased significantly both in mRNA and protein levels after PM2.5 exposure while the elevated secretory protein level of IL-1 beta in cell culture was detected by ELISA, which is one of the main downstream factors of NLRP1. In addition, the upregulation of NLRP1 and IL-1 beta could be reversed by NF-kappa B inhibitor indicating that PM2.5 may promote NLRP1 expression through activating NF-kappa B pathway. Furthermore, high ROS level was also found in cells treated with PM2.5 and inhibition of ROS could also reverse NK-kappa B production stimulated by PM2.5 that means ROS is involved in this skin inflammation process.