Biology: A new type of cell with regenerative capacity in human lungs

It was discovered by the University of Pennsylvania a new type of cell in the lungs human, which is capable of performing a key role in lung disease. The researchers analyzed human lung tissue to find new cells, called respiratory airway secretory cells. These cells line tiny branches of the airways near the alveolar structures where oxygen is exchanged for carbon dioxide.

These cells have stem cell-like properties that allow them to regenerate further cells essential for the regular functioning of the alveoli. They also found evidence that cigarette smoking and COPD chronic obstructive pulmonary disease, they can interrupt this regeneration process of these cells. This suggests that correcting this disruption could be a good way to treat this condition.

Biology, a new cell type with regenerative capabilities found

COPD is a devastating and common disease, but we don’t really understand the cellular biology of why or how some patients develop it. Identifying new cell types, particularly new progenitor cells, that are damaged in COPD could indeed accelerate the development of new treatments. It typically has progressive damage and loss of alveoli, exacerbated by chronic inflammation. It is estimated to affect around 10% of people e cause approximately 3 million deaths each year worldwide. ******* medications are prescribed, but these treatments can only slow down the disease process rather than stop or reverse it.

The new study uncovered evidence of these cells while examining gene activity signatures of lung cells sampled from healthy human donors. They soon recognized that the RASC, which do not exist in the lungs of the mouse, are secretory cells that reside near the alveoli and produce the proteins necessary for the fluid lining of the airways. Observations of the similarities in gene activity between RASC and an important progenitor cell in the alveoli called AT2 cells led the team to a further discovery: RASCs, in addition to their secretory function, serve as predecessors for AT2 cells, regenerating them to maintain the AT2 population and keep alveoli healthy.

AT2 cells become abnormal in COPD and other lung diseases, and the researchers found evidence that i defects in the RASCs could be an upstream cause of these anomalies. In the lung tissue of people with COPD, as well as people without COPD who have a history of smoking, they observed many AT2 cells that were altered in a way that suggested defective transformation from RASC to AT2. More research is needed at the moment, but the findings suggest the possibility of future treatments for this conditionrestoring the normal differentiation process from RASC to AT2 or even replenishing the normal RASC population in the damaged lungs.

Image by Ernesto Eslava from Pixabay