Inflammatory response in human lung cells stimulated with plasma from COPD patients.
COPD
CRP
IL-8
MMP-9
inflammation
Journal
Multidisciplinary respiratory medicine
ISSN: 1828-695X
Titre abrégé: Multidiscip Respir Med
Pays: Italy
ID NLM: 101477642
Informations de publication
Date de publication:
12 Jan 2022
12 Jan 2022
Historique:
received:
11
11
2021
accepted:
21
04
2022
entrez:
13
6
2022
pubmed:
14
6
2022
medline:
14
6
2022
Statut:
epublish
Résumé
Chronic obstructive pulmonary disease (COPD) is a condition resulting from a persistent inflammatory state in the airways even after smoking cessation. Intriguingly, the reasons behind this persistence of the inflammatory influx without smoking exposure have not been fully unraveled. We aimed to explore the hypothesis that systemic inflammation in COPD patients influences lung cell inflammatory response. We cultured human lung fibroblast and human airway epithelial cell lines with plasma from COPD patients (four emphysematous-COPD, four asthma-COPD overlap, four chronic bronchitis-COPD, and four bronchiectasis- COPD), and four smokers or ex-smokers without COPD as controls. Non-stimulated cells were used as controls. We measured Interleukine-8 (IL-8), C-reactive protein (CRP) and matrix metalloproteinase-9 (MMP-9) in plasma and culture supernatants by ELISA. Cells stimulated with plasma from COPD patients and non-COPD smoker subjects produced higher CRP, IL- 8 and MMP-9 levels, an increase for COPD in CRP (p=0.029) in epithelial cells and IL-8 (p=0.039) in fibroblasts and decrease for MMP-9 (p=0.039) in fibroblasts, compared with non-stimulated cells. The response was higher in epithelial cells for IL-8 (p=0.003) and in fibroblasts for MMP-9 (p=0.063). The plasma from chronic bronchitis and bronchiectasis phenotypes induced higher IL-8 in fibroblasts. Plasma from COPD patients increases the inflammatory response in lung epithelial cells and lung fibroblasts, with a different response depending on the cell type and clinical phenotype.
Sections du résumé
Background
UNASSIGNED
Chronic obstructive pulmonary disease (COPD) is a condition resulting from a persistent inflammatory state in the airways even after smoking cessation. Intriguingly, the reasons behind this persistence of the inflammatory influx without smoking exposure have not been fully unraveled. We aimed to explore the hypothesis that systemic inflammation in COPD patients influences lung cell inflammatory response.
Methods
UNASSIGNED
We cultured human lung fibroblast and human airway epithelial cell lines with plasma from COPD patients (four emphysematous-COPD, four asthma-COPD overlap, four chronic bronchitis-COPD, and four bronchiectasis- COPD), and four smokers or ex-smokers without COPD as controls. Non-stimulated cells were used as controls. We measured Interleukine-8 (IL-8), C-reactive protein (CRP) and matrix metalloproteinase-9 (MMP-9) in plasma and culture supernatants by ELISA.
Results
UNASSIGNED
Cells stimulated with plasma from COPD patients and non-COPD smoker subjects produced higher CRP, IL- 8 and MMP-9 levels, an increase for COPD in CRP (p=0.029) in epithelial cells and IL-8 (p=0.039) in fibroblasts and decrease for MMP-9 (p=0.039) in fibroblasts, compared with non-stimulated cells. The response was higher in epithelial cells for IL-8 (p=0.003) and in fibroblasts for MMP-9 (p=0.063). The plasma from chronic bronchitis and bronchiectasis phenotypes induced higher IL-8 in fibroblasts.
Conclusions
UNASSIGNED
Plasma from COPD patients increases the inflammatory response in lung epithelial cells and lung fibroblasts, with a different response depending on the cell type and clinical phenotype.
Identifiants
pubmed: 35692377
doi: 10.4081/mrm.2022.817
pmc: PMC9179873
doi:
Types de publication
Journal Article
Langues
eng
Pagination
817Informations de copyright
©Copyright: the Author(s).
Références
Am J Respir Cell Mol Biol. 2018 Jul;59(1):13-17
pubmed: 29522352
Respir Res. 2013 Feb 20;14:24
pubmed: 23425215
Thorax. 2006 Feb;61(2):115-21
pubmed: 16055612
Allergy. 2019 Jul;74(7):1249-1256
pubmed: 30834543
Thorax. 2015 Sep;70(9):822-9
pubmed: 26048404
Am J Respir Crit Care Med. 1995 Oct;152(4 Pt 1):1262-7
pubmed: 7551380
Int J Chron Obstruct Pulmon Dis. 2016 May 27;11:1129-37
pubmed: 27313452
Thorax. 2000 Jan;55(1):12-8
pubmed: 10607796
Am J Respir Crit Care Med. 2001 Sep 15;164(6):1008-11
pubmed: 11587987
Am J Respir Crit Care Med. 1998 Jun;157(6 Pt 1):1791-7
pubmed: 9620907
Respir Res. 2010 May 25;11:63
pubmed: 20500811
Arch Bronconeumol. 2017 Jun;53(6):324-335
pubmed: 28477954
Front Mol Biosci. 2015 May 13;2:19
pubmed: 25988186
Expert Rev Respir Med. 2014 Oct;8(5):547-59
pubmed: 25113142
ERJ Open Res. 2019 Feb 01;5(1):
pubmed: 30723727
Respirology. 2008 Jan;13(1):128-33
pubmed: 18197923
Am J Respir Crit Care Med. 2011 Apr 1;183(7):876-84
pubmed: 21057003
Am J Respir Crit Care Med. 1999 Apr;159(4 Pt 1):1298-307
pubmed: 10194181
Arch Bronconeumol. 2012 Jul;48(7):247-57
pubmed: 22561012
J Immunol Res. 2018 Feb 18;2018:2349045
pubmed: 29670919
PLoS One. 2016 Apr 22;11(4):e0150586
pubmed: 27104349
Am J Med. 2003 Jun 15;114(9):758-62
pubmed: 12829203
Eur Respir J. 2007 Sep;30(3):467-71
pubmed: 17504799
Proc Am Thorac Soc. 2009 Dec;6(8):638-47
pubmed: 20008867
BMC Pulm Med. 2014 May 30;14:95
pubmed: 24884805
Int J Chron Obstruct Pulmon Dis. 2019 Sep 03;14:2037-2046
pubmed: 31564851
Respir Res. 2011 Mar 22;12:34
pubmed: 21426578
Am J Respir Crit Care Med. 2010 Sep 1;182(5):598-604
pubmed: 20522794
Am J Respir Crit Care Med. 1996 Oct;154(4 Pt 1):1055-60
pubmed: 8887607
Yonsei Med J. 2019 May;60(5):407-413
pubmed: 31016901
Chin Med J (Engl). 2007 Sep 5;120(17):1511-6
pubmed: 17908460
Respir Med. 2016 Feb;111:54-9
pubmed: 26733230
Front Immunol. 2018 Jan 25;9:66
pubmed: 29422903
Eur J Med Res. 2009 Dec 7;14 Suppl 4:90-6
pubmed: 20156734
Am J Respir Crit Care Med. 2012 Nov 15;186(10):982-8
pubmed: 22983959
J Res Med Sci. 2016 Mar 15;21:12
pubmed: 27904558
Int J Med Sci. 2013 Jun 08;10(8):938-47
pubmed: 23801879
Thorax. 2004 Jul;59(7):574-80
pubmed: 15223864