By Carissa Wong.
There is a false colourCT Scan showing lungs and damaged tissue.
The science photo library is part of the GCA.
The drugs may help regenerate mouse lungs that have been damaged by cigarette smoke. The drugs could eventually be used to reverse lung damage in people with COPD, which has no cure.
Smoking, air pollution or genetics can cause COPD, which is the third leading cause of death after heart disease and stroke. It involves an excessive immune response that damages the lungs, leading to chest tightness and elevated mucus levels.
The problem with COPD is that we don't have a way of preventing the progression of the disease and the decline in lung function. We only have ways to treat symptoms, for example, using anti- inflammatory drugs or bronchodilators, which relax lung muscles and widen the airways.
COPD damages cells that normally regenerate the lining of the lungs, meaning they can't repair themselves. Stem cell implants, which provide a source of progenitor cells, have been the focus of previous efforts to treat this.
A drug-based treatment could be more convenient to use on a larger scale. To find out which genes were more or less active in the lung tissue of people with COPD and mice exposed to cigarette smoke, Gosens and his colleagues analysed data from people with COPD and mice exposed to cigarette smoke, as well as data from healthy people and mice.
The two drugs iloprost and mioprostol were used to treat high blood pressure in lung arteries and stomach ulcers, respectively.
The mice were exposed to cigarette smoke for four months. The lung progenitor cells were grown in a gel for 14 days in dishes with either one of the drugs or no drug.
The progenitor cells are placed in a gel and formed mini-lung structures known as organoids.
The team assessed how many organoids formed in the absence or presence of the drugs, and found that both drugs appeared to fully restore the progenitor cells, which decreased after exposure to cigarette smoke. During a week of cigarette smoke exposure, the team treated the mice with the drugs and found they had the same beneficial effect on lung cells.
Compared to other drugs that can support lung regeneration in animals, the big benefit of the drugs is that they are already used to treat other conditions.
The team found that the drugs work by reinstating the clock in lung cells, which are disrupted by smoke exposure.
Organoid formation can show the potential of cells, but more work is needed to confirm that the drugs kick-start the process.
The idea behind this work is wonderful. People are working on regenerating power using drugs in COPD. The model uses mice that are 20 years old, whereas typical COPD patients are around 50. The Medical University of Vienna, Austria's Rolf Ziesche says better models are needed to establish therapeutic potential.
Science Advances is a journal.
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