Delphinidin Activates NFAT and Induces IL-2 Production Through SOCE in T Cells |
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Authors: | Evelyn Jara María A. Hidalgo Juan L. Hancke Alejandra I. Hidalgo Sebastian Brauchi Luisa Nuñez Carlos Villalobos Rafael A. Burgos |
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Affiliation: | 1. Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, P.O. Box 567, Valdivia, Chile 2. Institute of Physiology, Faculty of Medicine, Universidad Austral de Chile, Valdivia, Chile 3. Spanish Research Council, Institute of Molecular Biology and Genetics, University of Valladolid, Valladolid, Spain
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Abstract: | Delphinidin is an anthocyanidin that possesses antioxidant and anti-inflammatory effects; however, some reports suggest that delphinidin has pro-inflammatory properties. For this reason, we assessed the effect of delphinidin on cytokine production in T cells. We demonstrated that delphinidin increased the cytosolic-free Ca2+ concentration by releasing Ca2+ from intracellular stores and increasing Ca2+ entry. The putative Ca2+ release activated Ca2+ (CRAC) channel inhibitors BTP2 and gadolinium reduced the calcium entry stimulated by the anthocyanidin. Delphinidin induced nuclear factor of activated T cells (NFAT) translocation and NFAT-Luc activity in Jurkat cells and was dependent on the CRAC channel and calcineurin pathway. Delphinidin increased the mRNA expression and production of IL-2 in Jurkat cells and was inhibited by BTP2 and cyclosporine A. Using peripheral blood lymphocytes, we demonstrated that delphinidin increased the production of IL-2 and IFN-γ and was inhibited by BTP2. Taken together, our results suggest that delphinidin exerts immunostimulatory effects on T cells by increasing cytokine production through CRAC channel and NFAT activation. |
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