COPD is characterised by inflammation of the lower airways and destruction of lung tissue that limit airflow and lung function. One of the major causes of disease progression, for which there are no effective treatments, is excess inflammatory mucus that blocks airways and prevents normal breathing.
The research, due to be published in the Journal of Clinical Investigation in September, shows that viruses could be a significant risk factor for COPD. Viruses can affect the cells that line the airways, leading to the long-term lung inflammation and mucus production that is typical of COPD.
The researchers explored the relationship between the short-term duration of most viral infections and long-term chronic inflammatory diseases such as COPD. They knew that a molecule called interleukin-13 (IL-13) was the key driver of excess production of chronic airway mucus after viral infection and traced the source of IL-13 to cells in the immune system. But until now, they did not know how this type of immune response could cause a long-term disease like COPD.
Michael J. Holtzman, MD, lead researcher, believes that monitoring IL-13 production will allow doctors to identify which patients would benefit from strategies to interrupt this process in the body and prevent the advancement of COPD. “We also provided the initial evidence that an additional stress or danger, such as smoking or pollution or even another infection, could cause these cells to release IL-33, which then stimulates immune cells to produce IL-13 and in turn the airway mucus typical of COPD and related respiratory diseases. It’s also possible that smoke exposure predisposes individuals to the development of these cells and, in turn, the susceptibility to exacerbation and progression of this type of disease.”
Learn about the factors that can cause lung disease and the ways to reduce your contact with them.
Sign up to our free monthly newsletter to get the latest information and research news on lung conditions, plus views from experts and patients! You can unsubscribe at any time.