NEW evidence highlights a distinct subset of patients with chronic obstructive pulmonary disease (COPD) who exhibit airway eosinophilia, characterised by heightened type 2 inflammation and a beneficial response to inhaled corticosteroid therapy.
In a post hoc analysis of the DISARM randomised controlled trial, researchers examined airway epithelial brushings from COPD patients with and without airway eosinophilia, defined as eosinophils accounting for more than 1% of leukocytes in bronchoalveolar lavage. RNA sequencing was performed to quantify gene expression related to type 1, type 2, and type 17 inflammation, as well as IL-13 and mast cell activation. Canonical pathway enrichment analyses were conducted at baseline and after 12 weeks of inhaled corticosteroid treatment to determine differential immune activity between groups.
Among the 58 participants, 38% had airway eosinophilia at baseline. This group demonstrated more severe airflow obstruction and greater radiographic emphysema than those without eosinophilia. Epithelial gene expression of type 2 inflammatory markers, IL-13, and mast cell-related genes was significantly higher in the eosinophilic group, while type 1 and type 17 signatures were comparable across both groups. Canonical pathway analysis revealed upregulation of type 2 immune response and asthma-related pathways in eosinophilic patients. After 12 weeks of inhaled corticosteroid treatment, the eosinophilic group showed a significant reduction in type 2 inflammation and mast cell gene expression, a change not observed in non-eosinophilic patients.
These findings indicate that airway eosinophilia marks a biologically distinct and corticosteroid-responsive subtype of COPD. Identifying this phenotype may allow for more precise, inflammation-targeted management of the disease.
Reference
Leung C et al. Transcriptomic profiling of the airway epithelium in COPD links airway eosinophilia to type 2 inflammation and corticosteroid response. Eur Respir J. 2025;65(5):2401875.
