Unraveling the Immune Landscape of Chronic Obstructive Pulmonary Disease: Insights into Inflammatory Cell Subtypes, Pathogenesis, and Treatment Strategies

Abstract

Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disorder characterized by persistent airway inflammation and progressive airflow limitation, resulting in a significant global health burden and high mortality. This narrative review synthesizes the current evidence on the roles of leukocyte subtypes—including neutrophils, monocytes, lymphocytes, eosinophils, and basophils—in the pathogenesis and clinical management of COPD. Relevant original studies and reviews are included, providing data on leukocyte functions, associated biomarkers, and therapeutic implications. Neutrophils contribute to airway damage and remodeling by releasing proteases and reactive oxygen species, particularly in response to environmental exposure such as cigarette smoke or air pollution. Lymphocytes, especially CD8⁺ T cells, drive chronic inflammation and immune dysregulation. Monocytes differentiate into macrophages that promote airway fibrosis and persistent inflammation, further impairing lung function. Eosinophils, though classically linked to asthma, are now recognized for their role in eosinophilic COPD, where they are associated with an increased exacerbation risk and corticosteroid responsiveness. Basophils, though less studied, may influence airway inflammation through interactions with eosinophils and cytokine release. Understanding these immune cell dynamics provides insights into the heterogeneity of COPD and highlights potential targets for precision therapy. Tailored interventions based on inflammatory phenotypes may improve clinical outcomes and advance personalized treatment strategies.