The study found that people with COPD have higher levels of the natural peptide LL‑37 in their lungs, and that this peptide can make lung cells release inflammation signals and die, which may worsen the disease. It suggests LL‑37 could be a future drug target, but doesn’t give any immediate ways to use or avoid it for health optimization.

Previous research has shown that innate immune system was more important than the acquired immune system in the pathogenesis of COPD. LL-37 is the only human cathelicidin identified so far. As an integral part of the innate immune system, besides antibacterial activity, its chemotactic activity, damage repairing, influencing apoptosis and its cytotoxicity are attracting people's attention. The aim of the present study was to evaluate role of LL-37 in the pathogenesis of COPD. ELISA and immunohistochemistry were applied to investigate the expression of LL-37 in induced sputum and lung tissue of COPD patients. Bronchial epithelial cell (BEP2D) and alveolar epithelial cell (A549) were treated with LL-37 synthesis polypeptide in vitro to assess the role of LL-37 in inflammation and apoptosis. We found that increased induced sputum levels of LL-37 in COPD patients were associated with airflow limitation, health status and exercise tolerance and the expressing intensity of LL-37 in both airway district and pulmonary alveoli area in COPD group significantly increased compared with control group. Through stimulation by CSE and LPS, the expression of LL-37 was increased in bronchial epithelial cell and alveolar epithelial cell. LL-37 synthesis polypeptide can promote the releasing of inflammatory factor IL-8 and induce apoptosis of bronchial epithelial cell and alveolar epithelial cell. This study suggested that LL-37 may play important role in the pathogenesis of COPD and may be a possible novel therapeutic target in COPD.