Researchers discover new cell type that may affect human lung disease. read here

Researchers analyzed human lung tissue To identify new cells, they are called respiratory airway secretory cells (RASCs). Cells line the small airway branches, deep in the lungs near the alveoli structures where the exchange of oxygen for carbon dioxide occurs.

Scientists showed that RASC has stem cell The property enables them to regenerate other cells that are necessary for the normal functioning of the alveoli. They also found evidence that cigarette smoking and a common smoking-related disease called chronic obstructive pulmonary disease (COPD) can disrupt the regenerative functions of the RASC – indicating that correcting this disruption is a key part of the treatment for COPD. could be a good way.

“COPD is a devastating and common disease, yet we don’t really understand the cellular biology of why or how some patients develop it. Identifying new cell types, in particular new progenitor cells, that contribute to COPD injured, can actually accelerate the development of new treatments,” study first author Maria Basile, MD, PhD, instructor of pulmonary medicine.

Features of COPD progressive damage Further damage to the alveoli, exacerbated by chronic inflammation. It is estimated to affect about 10 percent of people in some parts of the United States and causes about 3 million deaths each year worldwide.

Patients are often prescribed steroid anti-inflammatory drugs and/or oxygen therapy, but these treatments can only slow rather than stop or reverse the disease process. Progress in understanding COPD has been gradual because mice – the standard laboratory animal – have lungs that lack the key features of human lungs.

In the new study, Morris and his team uncovered evidence of RASC by examining the gene-activity signatures of lung cells taken from healthy human donors. They soon identified that RASCs, which are not present in mouse lungs, are “secretory” cells that reside near the alveoli and produce proteins needed for the fluid layer of the airways.

“With studies like these, we are beginning to understand exactly what is happening in this very prevalent disease, at the cell-biology level,” said senior author Edward Morris, PhD, Robinett Foundation Professor of Medicine, a professor at said. of Cell and Developmental Biology, and director of the Penn-Chop Lung Biology Institute at Penn Medicine.

The observation of gene-activity similarities between RASCs and an important progenitor cell in the alveoli called AT2 cells led the team to another discovery: RASCs, in addition to their secretory function, act as precursors for AT2 cells. are – reproduce them to maintain the AT2 population. And keep the alveoli healthy.

AT2 cells are known to be abnormal in COPD and other lung diseases, and researchers found evidence that defects in RASCs may 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 saw many AT2 cells, which were altered in such a way that a defective RASC-to-AT2 alteration was indicated.

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