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Author Spotlight: Investigating the Pathophysiology of Eosinophilic Esophagitis
Published on: May 10, 2024
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Targeted therapy in eosinophilic chronic obstructive pulmonary disease
Mathieu Fieldes1, Chloé Bourguignon1, Said Assou1
1IRMB, INSERM, Montpellier University Hospital, Montpellier, France.
ERJ Open Research
|April 15, 2021
Summary
Biologic agents targeting eosinophilic inflammation show promise for treating chronic obstructive pulmonary disease (COPD) with type 2 (T2) endotypes. These therapies may help manage lung function decline and exacerbations in specific COPD patient groups.
Area of Science:
- Pulmonology
- Immunology
- Pharmacology
Background:
- Chronic obstructive pulmonary disease (COPD) is a major global health issue characterized by airflow limitation and inflammation.
- Asthma, particularly type 2 (T2) high eosinophilic asthma, has seen advancements in targeted biologic therapies.
- COPD and asthma share pathophysiological mechanisms, with a significant overlap observed in eosinophilic airway inflammation within COPD patients.
Purpose of the Study:
- To review the rationale for using biologic agents in COPD.
- To assess the efficacy of these agents in T2-endotype COPD patients.
Main Methods:
- Literature review of studies on biologic agents targeting eosinophilic inflammation.
- Analysis of data concerning the role of eosinophilia in COPD progression and exacerbations.
- Examination of clinical trial results for monoclonal antibodies targeting IL-5, IL-4, and IL-13 in asthma and their potential application in COPD.
Main Results:
- Eosinophilic airway inflammation is present in approximately 40% of COPD patients.
- Eosinophilia is implicated in COPD lung function decline and exacerbations.
- Biologic agents targeting T2-endotype pathways have shown efficacy in asthma and are being investigated for COPD.
Conclusions:
- Targeting eosinophilic traits with biologic agents represents a potential therapeutic strategy for a subset of COPD patients.
- Further research is warranted to establish the efficacy and safety of these agents in T2-endotype COPD.
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