What You Should Know:
– University of Arizona (UArizona) researchers have been awarded a new $3.8M grant from the National Institutes of Health (NIH) to investigate whether low levels of a lung protein called CC16 can predict who will develop chronic obstructive pulmonary disease (COPD) decades before symptoms appear.
– The five-year study, funded by the National Institute of Allergy and Infectious Diseases, is led by Dr. Stefano Guerra, director of population science at the U of A Asthma and Airway Disease Research Center.
Unlocking the “Low-Flyer” Pathway to Lung Disease
COPD, a progressive lung disease, is traditionally linked to a decline in lung function from smoking or environmental exposure in adulthood. However, recent research, including work by Dr. Guerra, has identified a second pathway to COPD. In this “low-flyer” trajectory, nearly half of all COPD cases arise because individuals never achieve normal peak lung function in young adulthood. This means a person’s lungs start off smaller or weaker and remain vulnerable throughout life. Identifying people on this path early could enable preventive strategies long before the disease manifests.
Dr. Guerra stated that if researchers can pinpoint children at risk for early COPD, they might be able to intervene while they are still young to “push them onto a healthier lung growth path”. The ultimate hope is to prevent lung disease before it ever develops.
CC16: A Potential Biomarker for Early Intervention
The study, titled “CC16 in Childhood and Resilience to Early Airflow Limitation in Adult Life,” will analyze blood samples for CC16 levels from diverse population studies in North America and Europe, including the Tucson Children’s Respiratory Study in Arizona. Researchers will also collect airway samples to investigate genetic and molecular markers. CC16, or club cell secretory protein, is a natural shield produced by specialized cells in the airways that helps calm inflammation and protect lung tissue from irritants and pollutants. Researchers hypothesize that low CC16 levels during childhood could leave the lungs more susceptible to damage, setting the stage for chronic diseases later in life.
The current grant builds on Dr. Guerra’s previous research, which established CC16 as a potential biomarker for persistent asthma. That study found that children with low CC16 levels faced a significantly higher risk of ongoing asthma symptoms into adulthood. The new grant extends these findings to COPD, focusing on the link between early lung function deficits and lifelong disease risk.
