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ORIGINAL RESEARCH article
Front. Med.
Sec. Pulmonary Medicine
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1572291
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Background: There is published evidence that a modest increase in blood eosinophils during stable COPD indicates future risk for exacerbations and a potential utility of inhaled corticosteroids. This has been perceived as an argument for targeting systemic eosinophil mobilization to prevent exacerbations in COPD, even though there are no published data on systemic eosinophil mobilization during exacerbations in patients without allergy.Methods: We investigated long-term tobacco smokers (LTS: ≥10 pack-years) with COPD and chronic bronchitis (COPD-CB; GOLD stage 1-4; n=47) but no allergy; LTS without COPD and CB (LTS; n=10), and healthy never-smokers (HNS; n=10) during stable disease for crosssectional comparisons. For longitudinal comparisons, we followed the COPD-CB group for 15 months during stable disease and exacerbations, excluding samples affected by systemic corticosteroids. We quantified blood concentrations of eosinophils, the activity marker eosinophilic cationic protein (ECP) and the chemokine interleukin (IL)-4.Results: During stable disease, the concentrations of eosinophils were similar for the COPD-CB and the LTS group, although higher than in the HNS group. Additionally, the concentrations of ECP and IL-4 were similar for all groups. During exacerbations, however, the concentrations of eosinophils, ECP and IL-4 were not further increased, and there was even a mathematical trend towards a decrease for these concentrations.The clinical evidence presented here suggests that there is no additional mobilization of blood eosinophils by average during exacerbations in COPD patients with chronic bronchitis but no allergy. Thus, in this common phenotype, the immunological rationale for targeting systemic eosinophils during exacerbations remains unaccounted for, which motivates verification studies in large cohorts stratified for allergy and chronic bronchitis.
Keywords: biomarker, COPD, exacerbation, ECP, IL-4, systemic
Received: 06 Feb 2025; Accepted: 08 Apr 2025.
Copyright: © 2025 Andersson, Andelid, Brundin, Ekberg-Jansson and Lindén. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Anders Andersson, Sahlgrenska University Hospital, Gothenburg, Sweden
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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