Calcineurin, IRAK-1and MAPK Signaling Molecules Modulate Jurkat T Cell Release Inflammatory Factors Induced By Traffic-related PM2.5

Objective: To investigate how calcineurin，IRAK-1and MAPK signaling moleculesregulate Jurkat T cells to release inflammatory factors induced by traffic-relatedPM2.5, and provide experimental basis for the immunotoxicity mechanism.Methods: The activity of calciceurin (CaN) was determined by special kit; the mRNAexpression of IRAK-1was detected through QRT-PCR; the protein expressions ofp-ERK, p-JNK and p-38protein were detected by Western Blot; the levels of IL-1β,IL-2, TNF-a in cellular supernatant were measured by ELISA.Results：When Jurkat T cells were exposed to100g/mL of PM2.5for3h,6h and24hrespectively, the activity of CaN was the strongest at3h. As resting and activatedJurkat T cells were stimulated by different concentrations of PM2.5for3h, the mRNAexpression of IRAK-1increased in100g/mL and200g/mL of PM2.5groups,there was significant difference with the corresponding saline group, P <0.05. Restingand activated cells were stimulated by100g/mL of PM2.5for6h and24h, the geneexpression of IRAK-1was higher than the corresponding saline control group, P<0.05.Resting cells were incubated with different concentrations of PM2.5for24h and48h,the expression of p-ERK protein decreased with the dose of PM2.5increasing, p-ERKprotein expression in320g/mL PM2.5group was lower than saline group, thedifferences were statistically significant (P<0.05). The expression of p-JNK1andp-JNK2protein increased with the dose of PM2.5increasing, there was significantdifference (P<0.05) between320g/mL PM2.5group and saline group. Theexpression of p-38protein increased with the dose of PM2.5increasing, it wassignificant between80g/mL,320g/mL PM2.5groups and saline control group(P<0.05). p-JNK antagonist (SP600125) and p-38antagonist (SB203580) wereadded before exposure to traffic-related PM2.5, p-JNK2and p-38protein expressionwere lower compared with the normal exposure. The resting and activated cells werestimulated by PM2.5for3h,6h and24h, the IL-1β and TNF-α levels in cellularsupernatant in100g/mL of PM2.5were higher than the saline group, but the IL-2 level was lower than the saline group.Conclusions: CaN, IRAK-1, and MAPK signaling molecules can regulate the releaseof inflammatory factors of immune cells induced by traffic-related PM2.5.