&NA; Dendritic cells (DCs) comprise a system of highly professional antigen presenting cells (APCs) which connect innate and adaptive immunity by undergoing dramatic shift in their maturation state. Phytomedicine Echinacea… Click to show full abstract
&NA; Dendritic cells (DCs) comprise a system of highly professional antigen presenting cells (APCs) which connect innate and adaptive immunity by undergoing dramatic shift in their maturation state. Phytomedicine Echinacea purpurea extracts (EE) could modulate murine dendritic cell fate and function. However, the underlying mechanism of EE on DCs development and maturation remains limited. In this study, immature DCs were induced phenotypic maturation with up‐regulated expression of key accessory molecules and the phagocytic activity was decreased after being treated with EE (400 &mgr;g/ml) for 48 h. We found that TLR1/2, JNK, p38‐MAPK and NF‐&kgr;B pathways were activated following EE exposure. Notably, JNK activation was demonstrated to be associated with increased IFN‐&ggr; response while p38‐MAPK pathway exhibited immuno‐regulatory effects via induction of IL‐10 and TGF‐&bgr;1. Furthermore, it was verified that NF‐&kgr;B signaling was responsible for EE‐induced synthesis of IFN‐&ggr;, IL‐12 and TGF‐&bgr;1, but not for IL‐10 induction. These results indicate that EE have the immunomodulatory potency to promote both phenotypic and functional maturation of BMDCs via modulating the activation of JNK, p38‐MAPK and NF‐&kgr;B pathways. Our findings contributed to the current understanding of the immunoregulatory function of EE and the mechanism of DCs maturation. Graphical abstract Figure. No caption available. HighlightsEchinacea purpurea extracts (EE) promoted phenotypic maturation while reduced the phagocytic activity of BMDCs.JNK activation was associated with EE‐induced IFN‐&ggr; response.p38‐MAPK exhibited immuno‐regulatory effects via induction of IL‐10 and TGF‐&bgr;1 following EE exposure.NF‐&kgr;B was responsible for EE‐induced synthesis of IFN‐&ggr;, IL‐12 and TGF‐&bgr;1, but not for IL‐10 induction.
               
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