ADAM17 and related epithelial injury markers in bronchoalveolar lavage and blood distinguish COPD from controls
(2026) In Respiratory Medicine 251. p.1-10- Abstract
BACKGROUND: Chronic obstructive pulmonary disease (COPD) has many known dysregulated inflammatory proteins. A disintegrin and metalloproteinase 17 (ADAM17) is a protease that sheds several proteins involved in COPD pathogenesis. The aim was to investigate ADAM17, its phosphorylated form (pADAM17) and its substrates in bronchoalveolar lavage (BAL) and blood from COPD and control subjects. METHODS: Groups were matched by sex, age, BMI and smoking status to compare between COPD, smoking and never smoking control subjects. The expression of ADAM17 and pADAM17 was assessed using immunofluorescence in BAL cells (n = 6-13). Concentrations of soluble ADAM17 and its substrates were quantified using ELISA or Luminex in BAL fluid (BALF, n = 11-14)... (More)
BACKGROUND: Chronic obstructive pulmonary disease (COPD) has many known dysregulated inflammatory proteins. A disintegrin and metalloproteinase 17 (ADAM17) is a protease that sheds several proteins involved in COPD pathogenesis. The aim was to investigate ADAM17, its phosphorylated form (pADAM17) and its substrates in bronchoalveolar lavage (BAL) and blood from COPD and control subjects. METHODS: Groups were matched by sex, age, BMI and smoking status to compare between COPD, smoking and never smoking control subjects. The expression of ADAM17 and pADAM17 was assessed using immunofluorescence in BAL cells (n = 6-13). Concentrations of soluble ADAM17 and its substrates were quantified using ELISA or Luminex in BAL fluid (BALF, n = 11-14) and blood (n = 10-30). RESULTS: COPD BAL samples had more ADAM17+ and pADAM17+ cells than controls and intracellular localisations were observed in epithelial cells of subjects with a smoking history. These elevations coincided with higher concentrations of several of the ADAM17 substrates in BALF from Smokers and COPD subjects, most prominently was the increased BALF HB-EGF found in COPD but not Smokers. Other changes in blood were also mostly related to epithelial injury and repair. CONCLUSIONS: Our findings highlight an overabundance of ADAM17 and pADAM17 in COPD airways that is accentuated beyond smoking-induced changes. This broad catalytic-complex analysis has both combined individual biomarkers and discovered more novel disease-specific biomarkers that may all relate to the overarching functionality of ADAM17 in COPD, warranting further investigation into the role this enzyme plays in COPD pathogenesis.
(Less)
- author
- Lau, Carin E.
LU
; van der Burg, Nicole M.D.
LU
; Ankerst, Jaro
LU
; Bjermer, Leif
LU
and Tufvesson, Ellen
LU
- organization
- publishing date
- 2026-01-01
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- ADAM17, Bronchoalveolar lavage, COPD, Epithelial injury, pADAM17
- in
- Respiratory Medicine
- volume
- 251
- article number
- 108596
- pages
- 1 - 10
- publisher
- Elsevier
- external identifiers
-
- scopus:105026613966
- pmid:41421560
- ISSN
- 1532-3064
- DOI
- 10.1016/j.rmed.2025.108596
- language
- English
- LU publication?
- yes
- additional info
- Publisher Copyright: Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.
- id
- 442f1780-fc87-4a52-97fb-12c24030c5d7
- date added to LUP
- 2026-01-16 07:33:36
- date last changed
- 2026-01-30 08:53:20
@article{442f1780-fc87-4a52-97fb-12c24030c5d7,
abstract = {{<p>BACKGROUND: Chronic obstructive pulmonary disease (COPD) has many known dysregulated inflammatory proteins. A disintegrin and metalloproteinase 17 (ADAM17) is a protease that sheds several proteins involved in COPD pathogenesis. The aim was to investigate ADAM17, its phosphorylated form (pADAM17) and its substrates in bronchoalveolar lavage (BAL) and blood from COPD and control subjects. METHODS: Groups were matched by sex, age, BMI and smoking status to compare between COPD, smoking and never smoking control subjects. The expression of ADAM17 and pADAM17 was assessed using immunofluorescence in BAL cells (n = 6-13). Concentrations of soluble ADAM17 and its substrates were quantified using ELISA or Luminex in BAL fluid (BALF, n = 11-14) and blood (n = 10-30). RESULTS: COPD BAL samples had more ADAM17+ and pADAM17+ cells than controls and intracellular localisations were observed in epithelial cells of subjects with a smoking history. These elevations coincided with higher concentrations of several of the ADAM17 substrates in BALF from Smokers and COPD subjects, most prominently was the increased BALF HB-EGF found in COPD but not Smokers. Other changes in blood were also mostly related to epithelial injury and repair. CONCLUSIONS: Our findings highlight an overabundance of ADAM17 and pADAM17 in COPD airways that is accentuated beyond smoking-induced changes. This broad catalytic-complex analysis has both combined individual biomarkers and discovered more novel disease-specific biomarkers that may all relate to the overarching functionality of ADAM17 in COPD, warranting further investigation into the role this enzyme plays in COPD pathogenesis.</p>}},
author = {{Lau, Carin E. and van der Burg, Nicole M.D. and Ankerst, Jaro and Bjermer, Leif and Tufvesson, Ellen}},
issn = {{1532-3064}},
keywords = {{ADAM17; Bronchoalveolar lavage; COPD; Epithelial injury; pADAM17}},
language = {{eng}},
month = {{01}},
pages = {{1--10}},
publisher = {{Elsevier}},
series = {{Respiratory Medicine}},
title = {{ADAM17 and related epithelial injury markers in bronchoalveolar lavage and blood distinguish COPD from controls}},
url = {{http://dx.doi.org/10.1016/j.rmed.2025.108596}},
doi = {{10.1016/j.rmed.2025.108596}},
volume = {{251}},
year = {{2026}},
}