1. Department of Laboratory Medicine, Huashan Hospital, Shanghai Medical School, Fudan University, Shanghai, P. R. China.
2. Department of Dermatology, Huashan Hospital, Shanghai Medical School, Fudan University, Shanghai, P. R. China.
3. Shanghai Key Laboratory of Meteorology and Health, Shanghai Meteorological Service, Shanghai, 200030, China.
4. Department of Environmental Health, School of Public Health and the Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai, P. R. China.
5. Key Laboratory of Public Health Safety of the Ministry of Education and Key Laboratory of Health Technology Assessment of the Ministry of Health, School of Public Health, Fudan University, Shanghai, P. R. China.
6. Shanghai Key Laboratory of Meteorological and Health, Shanghai, P. R. China.
*These authors contributed equally to this study.
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-1β 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-1β could be reversed by NF-κB inhibitor indicating that PM2.5 may promote NLRP1 expression through activating NF-κB pathway. Furthermore, high ROS level was also found in cells treated with PM2.5 and inhibition of ROS could also reverse NK-κB production stimulated by PM2.5 that means ROS is involved in this skin inflammation process.
Keywords: PM2.5, Human Immortalized Epidermal Cells, Inflammasome, NF-κB, ROS