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Mucus clearance is the first defense of a normal airway against airborne pathogens and pollutants. However, mucus hypersecretion—an important feature of chronic obstructive pulmonary disease (COPD), especially the chronic bronchitis phenotype—contributes to disease pathology and mortality. Prescriptions of some mucoactive medications, e.g. N-acetylcysteine and carbocysteine, have proved beneficial for COPD management. Mucins are large-molecular-weight glycoproteins which constitute the major solid components of mucus, giving mucus its viscous and elastic properties and enabling its defensive function. Most-expressed in the airway are three membrane-tethered mucins (MUC1, MUC4, and MUC16) and three gel-forming secreted mucins (MUC2, MUC5AC, and MUC5B). Although over-expression of all these mucins has been observed or postulated in COPD lungs, none has been specifically evaluated as affecting COPD. Evidence regarding immunosuppressive, bacterial-adhesive, anti-inflammatory, and tumorigenic effects of MUC1 in other disease conditions suggests MUC1 may contribute to immune suppression, airway remodeling, mucus obstruction, bacterial colonization, and disruption of epithelium integrity in COPD. Regulation of mucin synthesis and secretion is increasingly well understood. Mucin over-expression in COPD is probably caused by a combination of microbial products, airborne pollutants, and mediators of inflammation. Further studies are needed to determine the individual function and regulatory signaling of each mucin in COPD airways, with the objectives of better understanding the disease mechanism and of developing novel therapeutics for COPD treatment.

The function of mucins in the COPD airway