Why is chitin accumulation in human lungs linked to age-related fibrosis, and what does this mean for chitinase-based therapies?

Why is chitin accumulation in human lungs linked to age-related fibrosis, and what does this mean for chitinase-based therapies?
Recent research reveals that chitin accumulation in respiratory tracts can drive age-related pulmonary fibrosis. In mice lacking acidic mammalian chitinase (AMCase), chitin from food, bedding, and airborne insect/fungal debris accumulates in alveolar lavage fluid, correlating with significant fibrosis. Restoring AMCase expression in lung tissue reduced chitin levels and fibrosis severity. Human patients with interstitial lung disease also showed elevated chitin in bronchoalveolar lavage fluid, suggesting impaired chitin clearance pathways. While human gastric juice does contain chitinase, activity varies widely — about 20% of Westerners show no detectable enzyme — and is inducible by dietary exposure to insects, fungi, or shrimp shells. However, even hydrolyzed chitin is poorly absorbed due to its high molecular weight and insolubility. This opens therapeutic avenues for enhancing chitinase activity in elderly fibrotic patients.