CF is caused by a mutation in the Cystic Fibrosis Transmembrane Conductance Regulator which results in airway surface liquid (ASL) dehydration, impaired muco-ciliary clearance and chronic pulmonary infection and inflammation leading to progressive lung destruction. Resolvin D1 (RvD1) is a Docosahexaenoic acid derived lipid mediator which effects the resolution of inflammation (1) and attenuates LPS induced lung inflammation by supressing NFΚB activation (2). NuLi-1 (normal genotype) and CuFi-1airway epithelial cells (Δ508/Δ508) were grown as polarised, differentiated bronchial epithelia. Cells were treated with vehicle control or RvD1 1nM or 100nM (30 mins for ASL / overnight for IL8 experiments). The ASL was stained with Texas red®-dextran and imaged by live-cell confocal fluorescence microscopy. IL8 secretion was induced by TNFα or heat inactivated P. aeruginosa. Apical IL8 concentration was measured by ELISA. ASL height measured 7.2µm in NuLi-1 cells. CuFi-1 cells demonstrated reduced ASL height at 5.8µm and disrupted architecture. RvD1 1nM and 100nM restored ASL height in CuFi-1 cells to7.1µm* and 8.1µm** respectively (*P<0.05/**P<0.01, Student t test). RvD1 100nM attenuated TNFα induced IL8 secretion by CuFi-1 cells. Resolvin D1 restores airway surface liquid architecture and attenuates pro-inflammatory IL8 secretion by CF bronchial epithelial cells, suggesting therapeutic potential in CF lung disease.