Study Background and Disease Burden
Chronic obstructive pulmonary disease (COPD) is a heterogeneous respiratory disorder characterized by persistent airflow limitation and a chronic inflammatory response in the airways and lung parenchyma. Globally, COPD is a leading cause of morbidity and mortality, posing a significant clinical and socioeconomic burden. Traditionally, neutrophilic inflammation dominates COPD pathology; however, a distinct subset of patients exhibits airway eosinophilia, defined by increased eosinophil counts in distal airways. This eosinophilic endotype overlaps with type 2 inflammatory pathways classically associated with asthma, implicating potential differential pathophysiology and therapeutic responses. Understanding the molecular signatures linked to airway eosinophilia could refine COPD phenotyping and guide personalized treatment strategies, particularly regarding the use of inhaled corticosteroids (ICS). Despite known clinical associations, the transcriptomic landscape of airway epithelium in eosinophilic COPD and its response to ICS remain poorly defined.