Inflammatory cells and remodeling in bronchial biopsies from COPD patients and controls
- PMID: 40526700
- PMCID: PMC12173230
- DOI: 10.1371/journal.pone.0326267
Inflammatory cells and remodeling in bronchial biopsies from COPD patients and controls
Abstract
Background: The understanding of inflammation and remodeling in the bronchial wall of COPD patients with varying disease severity remains incomplete.
Methods: 35 healthy controls and 47 volunteer COPD patients underwent bronchoscopy with bronchoalveolar lavage (BAL) and sampling by endobronchial biopsies in 2014-2015 as part of the MicroCOPD Study. Biopsies were embedded in glycol methyl acrylate (GMA) resin and examined by immunohistochemistry and staining for enumeration of CD3 + , CD4 + , CD8 + , CD20 + , CD68 + , EG2 + , and NE+ inflammatory cells, as well as endothelial cells (EN4) and smooth muscle actin (SMA). Mucus cells were stained by periodic acid-schiff (PAS), and toluidine blue to visualize the reticular basement membrane (RBM).
Results: The numbers of macrophages and eosinophils were higher, and vascularity increased in the submucosa in COPD patients compared with healthy controls. In healthy smokers there were lower numbers of lymphocytes (CD3 +, CD4 +, CD8 +, CD20+) than never smokers. However, COPD patients with GOLD I/II had higher numbers of eosinophils and larger smooth muscle area compared with GOLD III/IV. COPD exacerbations the last year, blood eosinophils, and use of inhaled corticosteroids did not affect levels of inflammation or remodeling.
Conclusion: Smoking alters inflammation in healthy controls, while specific patterns of macrophages, eosinophils, and vascularity distinguish COPD from non-COPD in bronchial biopsies.
Copyright: © 2025 Eagan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Conflict of interest statement
"Tomas Eagan declares research grant from GSK and lecture fees from Boehringer Ingelheim and AstraZeneca. Rune Nielsen declares grants from Sanofi and AstraZeneca. This does not alter our adherence to PLOS ONE policies on sharing data and materials."
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