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The current study was conducted to observe the effects of fine particulate matter (PM 2.5 ) on human keratinocyte cell line (HaCaT) cells. The potential mechanism linking PM 2.5 and skin was explored. HaCaT cells were cultured and then accessed in plate with PM 2.5 . Cell viability was tested by Cell Counting Kit-8. The mRNA and protein expression of Filaggrin, Loricrin, Involucrin, and Repetin were analyzed. The levels of Granulocyte-macrophage Colony Stimulating Factor, Thymic Stromal Lymphopoietin, Tumor Necrosis Factor-α, Interleukin-1α, and Interleukin-8 were detected in the supernatant of the HaCaT cell with enzyme-linked immunosorbent assay kits. Cell viability decreased with the increase in PM 2.5 . Compared with the control group, the protein expression of Filaggrin, Repetin, Involucrin, and Loricrin showed different expression patterns in PM 2.5 treatment groups. The level of Tumor Necrosis Factor-α, Thymic Stromal Lymphopoietin, Interleukin-1α, and Interleukin-8 significantly increased in the cells treated with PM 2.5 . Ambient PM 2.5 may increase the risk of eczema and other skin diseases. The relative mechanism may be associated with the impairment of the skin barrier and the elevation of inflammatory responses., Competing Interests: The authors declare no conflict of interest.

Aim: Common indoor pollutants, as fine particulate matter (PM2.5), can damage people's health and cause skin allergies. However, it remains unknown which common pollutants can lead to allergy, such as, in children atopic dermatitis, and what is the key molecule. This study aimed to investigate the thymic stromal lymphopoietin (TSLP) produced from keratinocytes after environmental pollutant stimulation. Methods: PAM212 cells were treated by several pollutants, including PM2.5, formaldehyde, m-xylene, and 1,2,4-trimethylbenzene, and tried to analyze their relationships. The mRNA expression level of TSLP was determined by qPCR. The protein level of TSLP was detected by ELISA analysis. Results: The mRNA expression of TSLP was significantly up-regulated when PAM212 cells were stimulated by PM2.5 at 25 μg/ml for 12 h. Meanwhile, the protein level of TSLP in culture supernatant was increased. However, TSLP protein production was not detected in culture supernatant treated with formaldehyde, m-xylene, and 1, 2, 4-trimethylbenzene. Conclusion: PM2.5 promotes the expression of TSLP and may aggravate allergic response using this pathway. [ABSTRACT FROM AUTHOR]