Emphysema is a condition that causes damage to the alveoli, the air sacs in your lungs. The walls of the damaged air sacs become stretched out and cause your lungs to get bigger. This makes it harder to move your air in and out. It is the most common form of the condition known as chronic obstructive pulmonary disease (COPD) and is typically triggered by long-term cigarette smoking. Estimates show that approximately 200 million people around the world are affected. Unfortunately, there is no cure for this disease of the lungs.
A study conducted by researchers at Weill Cornell Medicine and NewYork-Presbyterian found that specialized endothelial cells may hold the key to treating emphysema. Endothelial cells line the inner surface of blood vessels and have been shown to play an important role in protecting and restoring the health of key organs. Specifically, lung endothelial cells line the inner surface of the lung’s network of blood vessels.
As part of their research, the team studied lung tissue from human emphysema patients while also looking at lung issue from mice with an induced form of the disease. What they found that was that changes in the activity of certain genes in lung endothelial cells and the loss of those cells was associated with decreased lung function and other indicators of emphysema progression.
The researchers then infused mice with induced emphysema with healthy lung endothelial cells from genetically identical mice and the results were astounding. The team showed that they could prevent and/or reverse most of the lung damage that was seen in untreated mice. By contrast, injecting other cell types, including endothelial cells from other tissues, did not have the same effect.
The team believes that this treatment effect might have to do with differences in the molecules secreted by diseased versus healthy lung endothelial cells. To back up this claim, they found that lung endothelial cells in both humans and mice with emphysema showed sharp increases in production of LRG1, a molecule that promotes new blood vessel growth that has been linked to retinal and kidney diseases as well as some cancers. Additionally, when the researchers deleted the gene for LRG1 from lung endothelial cells in mice, the lungs were largely protected from the lung damage of induced emphysema, much as they had been by the endothelial cell therapy.
In a news release from Cornell, Dr. Alexandra Racanelli, a co-first author on this study and an instructor of medicine in the Division of Pulmonary and Critical Care Medicine at Weill Cornell Medicine and a pulmonologist at NewYork-Presbyterian/Weill Cornell Medical Center, had this to say about the results.
“Taken together, our data strongly suggest the critical role of endothelial cell function in mediating the pathogenesis of COPD/emphysema. Targeting endothelial cell biology by administering healthy lung endothelial cells and/or inhibiting the LRG1 pathway may therefore represent strategies of immense potential for the treatment of patients with advanced COPD or emphysema.”
The full study was published in the Journal of Experimental Medicine.