Fudosteine effects on mucin production

Background: Many chronic respiratory conditions are associated with mucin hypersecretion induced by underlying inflammation. Objective: To analyse the results of a preclinical study assessing the pathogenic mechanisms of mucin hyperproduction and the consequent in vivo and in vitro effects of fudosteine, a mucoactive agent. Methods/results: Both LPS and TNF-α increased MUC5AC mucin production in vivo and in vitro, respectively, and fudosteine was found to reduce it by partially interfering with the kinase-mediated inflammation pathway that activates the MUC5AC gene. Conclusions: Further preclinical testing in animal models with chronic airways inflammation is necessary.