Abstract
Abstract Resolvin E1 (RvE1) is a lipid mediator derived from ω3 polyunsaturated fatty acids that exert potent anti-inflammatory roles in several disease models. However, the precise underlying mechanism how RvE1 exerts its action in vivo remains largely unknown. In this study, we investigated the mechanisms of the anti-inflammatory effect of RvE1 using a contact hypersensitivity model. We found that administration of RvE1 significantly suppressed skin inflammation through a blockade of BLT1, a leukotriene B4 (LTB4) receptor, on dendritic cells (DCs). Live imaging of cutaneous DCs by two-photon microscopy revealed that RvE1 significantly impaired DC motility in the skin and migration to draining lymph nodes as well as antigen presentation ability in the skin. LTB4-BLT1 signaling induced actin formation in DCs and increased DC motility by activating Cdc42 and Rac1 through the PI3 kinase pathway, which was canceled by the administration of RvE1. Taken together, our results indicate that RvE1 attenuates cutaneous immune responses by inhibiting cutaneous DC functions through LTB4-BLT1 signaling blockade.
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