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1.
Arch Environ Contam Toxicol ; 68(1): 31-7, 2015 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-25194241

RESUMEN

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 [Ca(2+)]. In contrast, cytosolic free Ca(2+) concentration [Ca(2+)]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 [Ca(2+)]i generated by Orai1 and CaN-NFAT gene expression, TNF-α and IL-2 cytoplasmic concentrations may be altered.


Asunto(s)
Canales de Calcio/metabolismo , Calcio/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Interleucina-2/metabolismo , Material Particulado/toxicidad , Factor de Necrosis Tumoral alfa/metabolismo , Expresión Génica , Humanos , Células Jurkat , Factores de Transcripción NFATC/metabolismo , Proteína ORAI1 , Linfocitos T
2.
Wei Sheng Yan Jiu ; 42(5): 822-7, 2013 Sep.
Artículo en Chino | MEDLINE | ID: mdl-24218893

RESUMEN

OBJECTIVE: To explore the effects of traffic-related PM2.5 on interleukin-2 (IL-2) in Jurkat T cells and the regulatory action of calcium signaling pathway. METHODS: The cells were exposed to 100 microg/ml of PM2.5 for 3, 6 and 24 h. Normal saline group, blank filter group, calcium chelating agent EGTA group and the calcineurin antagonist cyclosporine A (CSA) group were as parallel control. The level of IL-2 was detected by ELISA kits, the mRNA expression of CaN, NFAT were determined by QRT-PCR. The nuclear distribution of NFAT was observed by immunofluorescence microscopy. RESULTS: The level of IL-2 in Jurkat T cells exposed to 100 microg/ml PM2.5 was significantly lower than parallel groups, but higher than PM2.5 + CSA group and PM2.5 + EGTA group (P < 0.05). With the increase of time, the releasing level of IL-2 appeared reducing trend in 100 microg/ml of PM2.5 group. The mRNA expression level of NFAT and CaN were higher than parallel groups, PM2.5 + CSA group and PM2.5 + EGTA group (P < 0.05). PM2.5 can induce NFAT protein with dephosphorylation and be activated, and NFAT protein can shift into nuclear. The level of IL-2 was negatively associated with the expression level of NFAT and CaN gene (P < 0.05). CONCLUSION: Traffic-related PM2.5 may inhibit the releasing of IL-2, Ca(2+)-CaN-NFAT signal pathway may involve in the regulation of IL-2.


Asunto(s)
Contaminantes Atmosféricos/toxicidad , Señalización del Calcio/fisiología , Interleucina-2/metabolismo , Material Particulado/toxicidad , Humanos , Células Jurkat , Factores de Transcripción NFATC/genética , Factores de Transcripción NFATC/metabolismo , Emisiones de Vehículos
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