Muco-obstructive airway diseases, such as cystic fibrosis (CF), primary ciliary dyskinesia (PCD), and chronic obstructive pulmonary disease (COPD), are characterized by decreased mucociliary clearance and increased mucus accumulation in the airways (1, 2). The respiratory tract mucosal barrier contains heavily glycosylated tethered and secreted mucins that prevent the adhesion of foreign particles and provide scaffolding for antibodies and other antimicrobial materials (3). In muco-obstructive diseases, secreted mucins become compacted and entangled due to hypersecretion and dehydration, which leads to abnormalities in mucin folding (2, 4). Of the secreted mucins, MUC5B is the most abundant in human airways (5). MUC5B is secreted from submucosal glands as linear strands and elongated through dimerization of disulfide linkages, creating the mucus mesh network (6–8). However, in muco-obstructive diseases including CF, mucin degradation is commonly observed due in part to persistent inflammation and infection. Bacteria and immune cells in the diseased airways contribute to mucin degradation through the release of proteases, resulting in an increased abundance of short MUC5B strands and compromising the function of the mucus layer (4, 9, 10). Compacted stagnant mucin creates a unique niche that allows for bacteria to access nutrients resulting from degraded airway proteins and use the compacted mucin mesh as scaffolding for aggregation and biofilm formation (1, 11–13).

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