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Background and Objectives Mucin is an important component of mucus that performs thefirst line of defense against inhaled pathogens and particles, lubrication of organs, and protectionof airway. It is hyper-secreted in inflammatory airway diseases and is associated withmorbidity and mortality of the affected patients. Resolvin, an autacoid of a specific lipid structure,exhibits anti-inflammatory property against inflammatory airway diseases although itseffects on mucin secretion by human airway epithelial cells have not yet been demonstrated. In this regard, we investigated the effects of Resolvin on lipopolysaccharide (LPS)-inducedmucin expression in human airway epithelial cells. Materials and Method In mucin-producing human NCI-H292 epithelial cells, the effectsand brief signaling pathways of Resolvin D1 (RvD1) and Resolvin E1 (RvE1) on the LPS-inducedMUC4, MUC5AC, and MUC5B expression were investigated using reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay and Western blot analysis. Results RvD1 attenuated LPS-induced MUC4, MUC5AC, and MUC5B mRNA expressionand protein production in human NCI-H292 cells while RvE1 did not. RvD1 significantlyblocked LPS-induced activated phosphorylation of extracellular signal-regulated kinase 1/2(ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) while RvE1 did not. Conclusion These results suggest that RvD1 attenuates LPS-induced MUC4, MUC5AC,and MUC5B expressions via ERK1/2 MAPK, p38 MAPK, and NF-κB signaling pathways inairway epithelial cells. Therefore, RvD1 may modulate the control of mucus-hypersecretion ininflammatory airway diseases.

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