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Traffic-Related PM2.5 Induces Cytosolic [Ca2+] Increase Regulated by Orai1, Alters the CaN-NFAT Signaling Pathway, and Affects IL-2 and TNF-α Cytoplasmic Levels in Jurkat T-Cells

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Abstract

The atmospheric particulate matter with a diameter less than or equal to 2.5 um (PM2.5) can result in increased immune system damage or diseases, however, the possible mechanism remains unclear. In this study, we used Jurkat T cells to determine the effects of PM2.5 on T cell-mediated adaptive immune response. Our results indicated that PM2.5 exposure increased intracellular calcium ion concentration [Ca2+]. In contrast, cytosolic free Ca2+ concentration [Ca2+]i significantly decreased in Jurkat T cells transfected with Orai1siRNA. In addition, we detected the level of interleukin (IL)-2 and tumor-necrosis factor (TNF)-α as well as other signalling molecules, including calcineurin (CaN) and NFATc2, a gene on 20q13.2 that encodes a member of the nuclear factor of activated T cells (NFAT), in the supernatant of cells exposed to PM2.5. The expression of NFATc2 protein increased in a time-dependent manner after exposure to PM2.5, but the activity of CaN decreased. NFATc2 was not consistent with IL-2 accumulation, thus indicating the involvement of other signals in the suppression of IL-2 accumulation. Our findings demonstrate that PM2.5 exposure in immune cells results in locally increased [Ca2+]i generated by Orai1 and CaN-NFAT gene expression, TNF-α and IL-2 cytoplasmic concentrations may be altered.

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Acknowledgments

This research program was supported by the National Natural Science Foundation of China (Grant No. 81072261) and the 2009 Shanxi Province College Outstanding Youth Scholarly Leaders project.

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The author declare that they have no competing interest.

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Correspondence to Zhi-Hong Zhang.

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Tong, GQ., Zhang, ZH., Zhao, Y. et al. Traffic-Related PM2.5 Induces Cytosolic [Ca2+] Increase Regulated by Orai1, Alters the CaN-NFAT Signaling Pathway, and Affects IL-2 and TNF-α Cytoplasmic Levels in Jurkat T-Cells. Arch Environ Contam Toxicol 68, 31–37 (2015). https://doi.org/10.1007/s00244-014-0077-8

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  • DOI: https://doi.org/10.1007/s00244-014-0077-8

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