Eosinophilic inflammation: a key player in COPD pathogenesis and progression

Abstract

Background: Chronic Obstructive Pulmonary Disease (COPD) remains a significant public health challenge due to its high morbidity and mortality rates. Emerging research has identified eosinophilic inflammation as a crucial factor in the pathogenesis and exacerbation of COPD, warranting a detailed exploration of its underlying mechanisms and therapeutic implications.

Objective: This review aims to elucidate the role of eosinophils in COPD, focusing on their contribution to airway remodeling, exacerbation frequency, and the inflammatory cascade.

Methods: We conducted a comprehensive literature review of recent studies that discuss the pathophysiological role of eosinophils in COPD and the clinical outcomes associated with modulating eosinophilic activity.

Results: Eosinophils contribute to COPD progression by releasing cytotoxic proteins and cytokines that intensify the inflammatory response and airway alterations. Targeting specific eosinophil-related cytokines with monoclonal antibodies or receptor antagonists may potentially reduce eosinophil counts, mitigate exacerbations, and improve patient outcomes.

Conclusion: Understanding eosinophilic involvement in COPD can facilitate the development of precision medicine approaches, offering more tailored and effective treatment options. Future research should continue to focus on the integration of eosinophil biomarkers in clinical practice to enhance therapeutic decisions and management strategies for COPD patients.

Keywords: Airway remodeling; asthma; emphysema; eosinophilia; precision medicine.

Figure 1.

Mechanism of Antigen-Induced alarmin release and subsequent immune response leading to airway hyperresponsiveness. Illustration of antigens inducing the release of alarmins including thymic stromal lymphopoietin (TSLP), eotaxin, and interleukin-33 (IL-33). The antigens are detected by dendritic cells, which in turn activate T-helper type 2 (Th2) cells and innate lymphoid cells (ILC2). The Th2 cells release cytokines, including IL-4, which promotes the infiltration of eosinophils. These eosinophils bind to vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on endothelial cells, facilitating their migration to the site of inflammation guided by eotaxin. This process leads to airway hyperresponsiveness, characterized by inflammation, fibrosis, and collagen deposition.