T Cell IFN-c Suppression Following Alcohol and Burn Injury Is Independent of miRNA155

miRNA155 has been implicated in normal T cell function and their differentiations into the Th1 subtype. We have shown that acute alcohol (ethanol) intoxication combined with burn injury suppresses T cell IFN-c release. Herein, we examined whether the decrease in IFN-c is resulted from altered expression of miRNA155 and transcription factors-NFAT, Tbx21, Jun and Fos- in T cells following ethanol and burn injury. Mice received ethanol (,3 g/Kg) 4 hours prior to,12.5 % total body surface area sham or burn injury and were sacrificed one day after injury. Splenic T cells were harvested and cultured with anti-CD3 (2 mg/ml) in the presence or absence of rIL-12 (10 ng/ml) or PMA (10 ng/ml) plus ionomycin (50 ng/ml) for 48 hours. We observed a significant decrease in miRNA155, NFAT, Tbx21, Jun and Fos expression as well as IFN-c release in T cells cultured with anti-CD3 following ethanol and burn injury compared with shams. The co-treatment of T cells with rIL-12 prevented the decrease in IFN-c and NFAT, Tbx21, Jun and Fos, but not miRNA155. In contrast, the co-treatment with PMA plus ionomycin normalized the expression of NFAT. It did not prevent the decrease in IFN-c, Tbx21, Jun, Fos and miRNA155. Finally, results obtained in miRNA155-/- mice did not show any change in T cell release of IFN-c or expression of nuclear factors compared to wildtype mice. Together, these findings suggest that while ethanol and burn injury decreases th