Analysis of PM2.5-induced cytotoxicity in human HaCaT cells based on a microfluidic system

- PM2.5-induced cytotoxicity in HaCaT cells was clarified on the molecular level.
- NF-κB and NALP3 were activated, resulting in inflammatory response in HaCaT cells.
- The platform allowed for 3D cell culture and high-throughput protein detection.

Human exposure to PM2.5 causes several adverse health effects. Skin is the first barrier against harmful environmental substances and can directly contact with PM2.5, but there is no study about PM2.5-induced cytotoxicity in human skin cells on the molecular level partially due to the shortcomings of traditional research methods. In present study, we established a microfluidic system including a cell culture chip integrated with a high-throughput protein microarray chip to investigate the mechanism of PM2.5-mediated cytotoxicity in human HaCaT cells. We found that PM2.5 was lodged inside the cytoplasm, mitochondria and nucleus of HaCaT cells by TEM. Flow cytometry analysis indicated that the cell apoptosis rate increased from 0.49% to 53.4%. The results of protein microarray showed that NF-κB and NALP3 signal transductions were activated in HaCaT cells after PM2.5 stimulations, up-regulating the expression of IL-1β and IL-6, which resulted in inflammatory response in HaCaT cells. Our findings provide a molecular insight into PM2.5-induced skin injury.

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