Laura A. Hancock et al found evidence suggesting that impaired clearance of mucus in lungs due to overexpression of MUC5B gene may lead to pulmonary fibrosis, identifying it as a potential therapeutic target. Researchers reveal that the MUC5B, a mucin thought to be restricted to conducting airways, is co-expressed with surfactant protein C (SFTPC) in the type-2 alveolar epithelium in humans, indicating their role in developing idiopathic pulmonary fibrosis (IPF). Overexpression of Muc5b in a fibrosis induced mice model showed a reversal effect in the presence of mucolytic agent P-2119. With mucolytic agent, the mucociliary clearance (MCC) was restored with acute clearance of inflammatory cells from the lungs. The findings suggest that targeting MUC5B in the terminal airways of patients with preclinical stages of interstitial lung disease represents a rational strategy to prevent the progression of pulmonary fibrosis.
Source: Nature Communications volume 9, Article number: 5363 (2018) https://www.nature.com/articles/s41467-018-07768-9#Sec6 18 December 2018