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Central airways remodeling in COPD patients
BACKGROUND: The contribution to airflow obstruction by the remodeling of the peripheral airways in chronic obstructive pulmonary disease (COPD) patients has been well documented, but less is known about the role played by the large airways. Few studies have investigated the presence of histopatholog...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove Medical Press
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159070/ https://www.ncbi.nlm.nih.gov/pubmed/25214779 http://dx.doi.org/10.2147/COPD.S52478 |
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author | Pini, Laura Pinelli, Valentina Modina, Denise Bezzi, Michela Tiberio, Laura Tantucci, Claudio |
author_facet | Pini, Laura Pinelli, Valentina Modina, Denise Bezzi, Michela Tiberio, Laura Tantucci, Claudio |
author_sort | Pini, Laura |
collection | PubMed |
description | BACKGROUND: The contribution to airflow obstruction by the remodeling of the peripheral airways in chronic obstructive pulmonary disease (COPD) patients has been well documented, but less is known about the role played by the large airways. Few studies have investigated the presence of histopathological changes due to remodeling in the large airways of COPD patients. OBJECTIVES: The aim of this study was to verify the presence of airway remodeling in the central airways of COPD patients, quantifying the airway smooth muscle (ASM) area and the extracellular matrix (ECM) protein deposition, both in the subepithelial region and in the ASM, and to verify the possible contribution to airflow obstruction by the above mentioned histopathological changes. METHODS: Biopsies of segmental bronchi spurs were performed in COPD patients and control smoker subjects and immunostained for collagen type I, versican, decorin, biglycan, and alpha-smooth muscle actin. ECM protein deposition was measured at both subepithelial, and ASM layers. RESULTS: The staining for collagen I and versican was greater in the subepithelial layer of COPD patients than in control subjects. An inverse correlation was found between collagen I in the subepithelial layer and both forced expiratory volume in 1 second and ratio between forced expiratory volume in 1 second and forced vital capacity. A statistically significant increase of the ASM area was observed in the central airways of COPD patients versus controls. CONCLUSION: These findings indicate that airway remodeling also affects the large airways in COPD patients who have greater deposition of ECM proteins in the subepithelial layer and a larger smooth muscle area than control smoker subjects. These changes may contribute to chronic airflow obstruction in COPD patients. |
format | Online Article Text |
id | pubmed-4159070 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-41590702014-09-11 Central airways remodeling in COPD patients Pini, Laura Pinelli, Valentina Modina, Denise Bezzi, Michela Tiberio, Laura Tantucci, Claudio Int J Chron Obstruct Pulmon Dis Original Research BACKGROUND: The contribution to airflow obstruction by the remodeling of the peripheral airways in chronic obstructive pulmonary disease (COPD) patients has been well documented, but less is known about the role played by the large airways. Few studies have investigated the presence of histopathological changes due to remodeling in the large airways of COPD patients. OBJECTIVES: The aim of this study was to verify the presence of airway remodeling in the central airways of COPD patients, quantifying the airway smooth muscle (ASM) area and the extracellular matrix (ECM) protein deposition, both in the subepithelial region and in the ASM, and to verify the possible contribution to airflow obstruction by the above mentioned histopathological changes. METHODS: Biopsies of segmental bronchi spurs were performed in COPD patients and control smoker subjects and immunostained for collagen type I, versican, decorin, biglycan, and alpha-smooth muscle actin. ECM protein deposition was measured at both subepithelial, and ASM layers. RESULTS: The staining for collagen I and versican was greater in the subepithelial layer of COPD patients than in control subjects. An inverse correlation was found between collagen I in the subepithelial layer and both forced expiratory volume in 1 second and ratio between forced expiratory volume in 1 second and forced vital capacity. A statistically significant increase of the ASM area was observed in the central airways of COPD patients versus controls. CONCLUSION: These findings indicate that airway remodeling also affects the large airways in COPD patients who have greater deposition of ECM proteins in the subepithelial layer and a larger smooth muscle area than control smoker subjects. These changes may contribute to chronic airflow obstruction in COPD patients. Dove Medical Press 2014-09-01 /pmc/articles/PMC4159070/ /pubmed/25214779 http://dx.doi.org/10.2147/COPD.S52478 Text en © 2014 Pini et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Pini, Laura Pinelli, Valentina Modina, Denise Bezzi, Michela Tiberio, Laura Tantucci, Claudio Central airways remodeling in COPD patients |
title | Central airways remodeling in COPD patients |
title_full | Central airways remodeling in COPD patients |
title_fullStr | Central airways remodeling in COPD patients |
title_full_unstemmed | Central airways remodeling in COPD patients |
title_short | Central airways remodeling in COPD patients |
title_sort | central airways remodeling in copd patients |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159070/ https://www.ncbi.nlm.nih.gov/pubmed/25214779 http://dx.doi.org/10.2147/COPD.S52478 |
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