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New Cell Type With Regenerative Properties Discovered in Human Lung

Researchers have identified a distinct secretory cell lineage deep within human lungs that has a critical role in maintaining the gas-exchange compartment and is altered in chronic lung disease.

The newly-identified lung cells, named respiratory airway secretory cells (RASCs), line tiny airway branches near the alveoli structures where oxygen is exchanged for carbon dioxide. They have stem-cell-like properties enabling them to regenerate other cells that are essential for the normal functioning of alveoli.

The researchers found evidence that cigarette smoking and the common smoking-related ailment called chronic obstructive pulmonary disease (COPD) can disrupt the regenerative functions of these cells — hinting that correcting this disruption could be a good way to treat COPD.

“COPD is a devastating and common disease, yet we really don’t understand the cellular biology of why or how some patients develop it,” said Dr. Maria Basil, a researcher in the Department of Medicine and the Penn-CHOP Lung Biology Institute at the University of Pennsylvania’s Perelman School of Medicine.

Identifying new cell types, in particular new progenitor cells, that are injured in COPD could really accelerate the development of new treatments.

In their study, Dr. Basil and her colleagues uncovered evidence of RASCs while examining gene-activity signatures of lung cells sampled from healthy human donors.

They soon recognized that RASCs, which don’t exist in mouse lungs, are secretory cells that reside near alveoli and produce proteins needed for the fluid lining of the airway.

With studies like this we’re starting to get a sense, at the cell-biology level, of what is really happening in this very prevalent disease, said Professor Edward Morrisey, director of the Penn-CHOP Lung Biology Institute at the University of Pennsylvania’s Perelman School of Medicine.

Observations of gene-activity similarities between RASCs and an important progenitor cell in 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 are known to become abnormal in COPD and other lung diseases, and the authors found evidence that defects in RASCs might be an upstream cause of those abnormalities.

In lung tissue from people with COPD, as well as from people without COPD who have a history of smoking, they observed many AT2 cells that were altered in a way that hinted at a faulty RASC-to-AT2 transformation.

More research is needed, but the findings point to the possibility of future COPD treatments that work by restoring the normal RASC-to-AT2 differentiation process — or even by replenishing the normal RASC population in damaged lungs.

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