ew research performed in mice models at Penn Medicine shows, mechanistically, how the infant lung regenerates cells after injury differently than the adult lung, with alveolar type 1 (AT1) cells reprograming into alveolar type 2 (AT2) cells (two very different lung alveolar epithelial cells), promoting cell regeneration, rather than AT2 cells differentiating into AT1 cells, which is the most widely accepted mechanism in the adult lung. These study findings, published today in Cell Stem Cell, show that the long-held assumption that AT1 and AT2 cells behave the same way in children and in adults is untrue.
The lung alveolus is where gas is exchanged between the environment and blood. While scientists have known about two very different lung alveolar epithelial cells since the 1940s, there had not been much insight into them on a molecular level before now. Furthermore, these findings reveal the molecular pathway that allows for this transformation. The Penn researchers also showed that by turning off this pathway, they could reprogram adult AT1 cells into AT2 cells. This unveils a previously unappreciated level of age-dependent cell plasticity, which could explain, in part, why pediatric lungs are not as heavily impacted by COVID-19 as adult lungs, and is a major step forward in understanding lung regeneration as a form of lung therapy.
