Abstract
Chronic obstructive pulmonary disease (COPD) is a common and preventable airway disease causing significant worldwide mortality and morbidity. Lifetime exposure to tobacco smoking and environmental particles are the two major risk factors. Over the last decades, COPD has become a growing public health problem with an increase in incidence. COPD is defined by airflow limitation due to airway inflammation and small airway remodelling coupled to parenchymal lung destruction. Most patients exhibit neutrophil-predominant airway inflammation combined with an increase in macrophages and CD8+ T-cells. Asthma is a heterogeneous chronic inflammatory airway disease. The most studied subtypes is T2 high eosinophilic asthma, for which there are an increasing number of biologic agents developed. However, both asthma and COPD are complex and share common pathophysiologic mechanisms. They are known as overlapping syndromes as approximately 40% of patients with COPD present an eosinophilic airway inflammation. Several studies suggest a putative role of eosinophilia in lung function decline and COPD exacerbation. Recently, pharmacological agents targeting eosinophilic traits in uncontrolled eosinophilic asthma, especially monoclonal antibodies directed against interleukins (IL5, IL4, IL13) or their receptors, have shown promising results. This review examines data on the rationale for such biological agents and assesses efficacy in T2-endotype COPD patients.
Footnotes
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Conflict of interest: Dr. FIELDES has nothing to disclose.
Conflict of interest: Dr. Bourguignon has nothing to disclose.
Conflict of interest: Dr. Assou has nothing to disclose.
Conflict of interest: Dr. Nasri has nothing to disclose.
Conflict of interest: Dr. Petit has nothing to disclose.
Conflict of interest: Dr. Vachier has nothing to disclose.
Conflict of interest: Dr. De Vos has nothing to disclose.
Conflict of interest: Dr. Ahmed has nothing to disclose.
Conflict of interest: Dr. Bourdin reports grants, personal fees, non-financial support and other from AstraZeneca, grants, personal fees, non-financial support and other from Boeringher Ingelheim , grants, personal fees, non-financial support and other from GlaxoSmithKline, personal fees, non-financial support and other from Novartis, personal fees and non-financial support from Teva, personal fees, non-financial support and other from Regeneron, personal fees, non-financial support and other from Chiesi Farmaceuticals, grants, personal fees, non-financial support and other from Actelion, personal fees from Gilead, non-financial support and other from Roche, other from Nuvaira, from null outside the submitted work;.
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- Received June 26, 2020.
- Accepted December 14, 2020.
- Copyright ©ERS 2021
This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.
