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Background  We have previously found that reactive oxygen species (ROS) are involved in  Pseudomonas aeruginosa  lipopolysaccharide ( PA-LPS ) induced MUC5AC in airway epithelial cells. Dual oxidase1 (Duox1), a member of NADPH oxidase(Nox), is known to be responsible for ROS production in respiratory tract epithelial cells. Our aim was to clarify whether Duox1 was also involved in the  PA-LPS -induced MUC5AC and calcium dependent chloride channel 3(Clca3), another recognized marker of goblet cell hyperplasia and mucus hyper-production.    Methods    PA-LPS -induced Duox1 mRNA levels were examined in A549 cells, primary mouse tracheal epithelial cells (mTECS) and lung tissues of mice. Nox inhibitors diphenyleneiodonium chloride (DPI) and Duox1 siRNA were used to investigate whether Duox1 is involved in  PA-LPS -induced MUC5AC and Clca3 expression both in vitro and in vivo.    Results  Duox1 is induced by  PA-LPS  in A549 cells, primary mTECs and lung tissues of mice. DPI significantly inhibited  PA-LPS -induced up-regulation of Duox1, Muc5ac and Clca3 in primary mouse trachea epithelial cells and lung tissues of mice. Knockdown of Duox1 markedly inhibited  PA-LPS -induced MUC5AC expression via a ROS-TGF-α cascade in A549 cells. Furthermore, DPI significantly inhibited  PA-LPS -induced increases in inflammatory cells accumulated in mouse lungs.    Conclusions  We demonstrate for the first time that  PA-LPS -induced MUC5AC and Clca3 expression is partly through Duox1, and provide supportive evidence for Duox1 as a potential target in treatments of mucin over-production diseases.

P. aeruginosa Lipopolysaccharide-Induced MUC5AC and CLCA3 Expression Is Partly through Duox1 In Vitro and In Vivo