In a recent study published in the journal Lancet Respiratory Medicine, a team of researchers found that low concentrations of CC16 in serum are associated with reduced lung function in childhood, accelerated lung function decline in adulthood and development of moderate airflow limitation in the general adult population.
“That we found this association in people without COPD suggests that the relation between low CC16 concentration and decline in [forced expiratory volume in 1 second (FEV1)] is established before disease inception,” wrote Stefano Guerra, MD, PhD, MPH, a research associate professor of medicine at The University of Arizona, Tucson, along with colleagues.
The development of chronic obstructive pulmonary disease (COPD) in smokers and their susceptibility to infections is not fully understood. Recent evidence suggests that Clara cells play a part in host defense, immunomodulatory response and airway remodeling through the production of specific factors such as Clara cell 16 (CC-16).
To assess the effects of CC16 concentration in 960 adults without COPD, in the study titled ”Relation between circulating CC16 concentrations, lung function, and development of chronic obstructive pulmonary disease across the lifespan: a prospective study,” Stefano Guerra from the Arizona Respiratory Center, University of Arizona and colleagues used data from the Tucson Epidemiological Study of Airway Obstructive Disease.
The researchers also tested for replication of results using data retrieved from the European Community Respiratory Health Survey ([ECRHS-Sp] n=514, 11 years), and Swiss Cohort Study on Air Pollution and Lung Diseases in Adults ([SAPALDIA] n=167, 8 years) studies.
After adjustment for sex, age, height, smoking status and intensity, pack-years, asthma, and FEV1 at baseline, the team of researchers found an inverse association between CC16 concentration and decline in FEV1 in adults in TESAOD and ECRHS-Sp; the effect in SAPALDIA was marginal.
Results also showed that low CC16 concentration at baseline was associated with increased risk of incident stage 2 airflow limitation in TESAOD and ECRHS-Sp.
In children, the lowest tertile of CC16 concentrations was associated with a subsequent FEV1 deficit of 68 mL up to age 16 years, which was confirmed in children who had never smoked by age 16 years.
According to the researchers, “Long-term studies that can control for such physiological factors and model serial CC16 measurements are needed to establish conclusively the potential of this molecule as a biomarker for prevention of treatment of COPD, whether in the general population or targeted subgroups.”