New research shows that vitamin A that plays a key role in lung development and maintenance, and may play a protective role in lung injury caused by cigarette smoke exposure and viral infections.
It’s no surprise that smoking is bad for the lungs. But only 10%-20% of long-term smokers will develop serious conditions that affect breathing, such as emphysema and chronic obstructive pulmonary disease (COPD). To understand why, a Yale-led team studied the mechanisms that cause lung health to decline.
Led by assistant professor of medicine (pulmonary, critical care and sleep medicine) Dr. Charles S. Dela Cruz, the researchers focused on retinoic acid, a form of vitamin A that plays a key role in lung development and maintenance. By studying mouse models, the researchers found that exposure to cigarette smoke causes a key protein, IL-15, to significantly weaken a retinoic acid receptor. That weakening is further exacerbated by viral infections, which tend to be more severe in people with COPD.
The finding provides researchers with a strategy to restore retinoic acid’s protective function and decrease lung damage. With this insight, scientists can develop potential therapies for patients suffering from emphysema and COPD, a leading cause of death in the United States.
The study appeared in April 29 in American Journal of Respiratory Cell Molecular Biology.
Reference: “Interleukin-15 Regulates Retinoic Acid Receptor Beta in the Lung During Cigarette Smoking and Influenza Virus Infection” by Jianmiao Wang, Wei Liu, Chad Marion, Rajvir Singh, Nathaniel Andrews, Chun Geun Lee, Jack A. Elias and Charles S. Dela Cruz, 29 Apr 2015, American Journal of Respiratory Cell Molecular Biology.
DOI: 10.1165/rcmb.2014-0448OC
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