CU researchers have created a transgenic mouse model that overexpresses a major gel-forming mucin, Muc5b, in the lungs. To drive tissue-specific expression, the coding region of Muc5b is under control of the rat secretoglobin 1a1 (Scgb1a1) promoter. Evidence from human patient samples combined with this mouse model have been used demonstrate that excess Muc5b in the lungs is a dominant risk factor for idiopathic pulmonary fibrosis (IPF). These transgenic mice present with impaired mucociliary clearance and increased lung fibrosis in models of lung injury. This creates an excellent rodent model to study the molecular pathology of IFP and to test investigational drugs to treat the disease.
Hancock LA, Hennessy CE, Solomon GM, et al. Muc5b overexpression causes mucociliary dysfunction and enhances lung fibrosis in mice. Nature Communications. 2018;9(1):5363.