Background
Chronic obstructive pulmonary disease (COPD) is currently listed as the 3rd leading cause of death in the United States. COPD is marked by limitations in expiratory airflow, emphysematous destruction of the lungs, bronchitis, and chronic inflammation of the lung tissue. With the emerging prevalence in usage of electronic nicotine delivery systems (ENDS), the impact of ENDS on the development of lung diseases such as COPD requires further attention. Previous studies have shown that β-epithelial Na+ channel (βENaC)- overexpressing mice have multiple emphysematous phenotypes, such as mucus accumulation and chronic inflammation. This study was aimed to elucidate the effects of e-cigarettes, a type of ENDS, on the development of COPD.
Methods
We hypothesized that acute repetitive usage of ENDS will exacerbate the features of COPD including mucus production, inflammation, and fibrosis, ultimately leading to lung injury. Twenty βENaC mice (10 mice per group) underwent whole body ENDS or sham air exposure for 2 hours daily over 10 days. Bronchoalveolar lavage (BAL) fluid and lung tissues were collected to assess for inflammation, fibrosis, mucus accumulation, and alveolar damage.
Results and Discussion
Our data showed that ENDS exposure significantly increased the alveolar size as compared with the control. We also found that level of inflammatory cytokines, such as CCL2, IL-13, and IL-10, were elevated in animals exposed to ENDS compared with control. Moreover, we observed ENDS exposure caused mucus accumulation, alveolar destruction, and fibrosis in the bronchioles of the βENaC mice. Additionally, ENDS exposure promoted apoptosis in pulmonary endothelial cell and epithelial cells.
Conclusion
Our data suggest that nicotine-containing e-cigarettes exacerbates features of COPD involving abnormal lung inflammation, mucus accumulation and apoptosis in βEnaC mice.