Susceptibility for cigarette smoke-induced DAMP release and DAMP-induced inflammation in COPD.
Pouwels, SD
Hesse, L
Faiz, A
Lubbers, J
Bodha, PK
Ten Hacken, NHT
van Oosterhout, AJM
Nawijn, MC
Heijink, IH
- Publisher:
- AMER PHYSIOLOGICAL SOC
- Publication Type:
- Journal Article
- Citation:
- Am J Physiol Lung Cell Mol Physiol, 2016, 311, (5), pp. L881-L892
- Issue Date:
- 2016-11-01
Closed Access
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ajplung.00135.2016.pdf | Published version | 2.34 MB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Pouwels, SD | |
dc.contributor.author | Hesse, L | |
dc.contributor.author |
Faiz, A https://orcid.org/0000-0003-1740-3538 |
|
dc.contributor.author | Lubbers, J | |
dc.contributor.author | Bodha, PK | |
dc.contributor.author | Ten Hacken, NHT | |
dc.contributor.author | van Oosterhout, AJM | |
dc.contributor.author | Nawijn, MC | |
dc.contributor.author | Heijink, IH | |
dc.date.accessioned | 2022-07-29T22:24:40Z | |
dc.date.available | 2016-09-06 | |
dc.date.available | 2022-07-29T22:24:40Z | |
dc.date.issued | 2016-11-01 | |
dc.identifier.citation | Am J Physiol Lung Cell Mol Physiol, 2016, 311, (5), pp. L881-L892 | |
dc.identifier.issn | 1040-0605 | |
dc.identifier.issn | 1522-1504 | |
dc.identifier.uri | http://hdl.handle.net/10453/159380 | |
dc.description.abstract | Cigarette smoke (CS) exposure is a major risk factor for chronic obstructive pulmonary disease (COPD). We investigated whether CS-induced damage-associated molecular pattern (DAMP) release or DAMP-mediated inflammation contributes to susceptibility for COPD. Samples, including bronchial brushings, were collected from young and old individuals, susceptible and nonsusceptible for the development of COPD, before and after smoking, and used for gene profiling and airway epithelial cell (AEC) culture. AECs were exposed to CS extract (CSE) or specific DAMPs. BALB/cByJ and DBA/2J mice were intranasally exposed to LL-37 and mitochondrial (mt)DAMPs. Functional gene-set enrichment analysis showed that CS significantly increases the airway epithelial gene expression of DAMPs and DAMP receptors in COPD patients. In cultured AECs, we observed that CSE induces necrosis and DAMP release, with specifically higher galectin-3 release from COPD-derived compared with control-derived cells. Galectin-3, LL-37, and mtDAMPs increased CXCL8 secretion in AECs. LL-37 and mtDAMPs induced neutrophilic airway inflammation, exclusively in mice susceptible for CS-induced airway inflammation. Collectively, we show that in airway epithelium from COPD patients, the CS-induced expression of DAMPs and DAMP receptors in vivo and the release of galectin-3 in vitro is exaggerated. Furthermore, our studies indicate that a predisposition to release DAMPs and subsequent induction of inflammation may contribute to the development of COPD. | |
dc.format | Print-Electronic | |
dc.language | eng | |
dc.publisher | AMER PHYSIOLOGICAL SOC | |
dc.relation.ispartof | Am J Physiol Lung Cell Mol Physiol | |
dc.relation.isbasedon | 10.1152/ajplung.00135.2016 | |
dc.rights | info:eu-repo/semantics/closedAccess | |
dc.subject | 0606 Physiology, 1116 Medical Physiology | |
dc.subject.classification | Respiratory System | |
dc.subject.mesh | Administration, Intranasal | |
dc.subject.mesh | Adult | |
dc.subject.mesh | Alarmins | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Antimicrobial Cationic Peptides | |
dc.subject.mesh | Cathelicidins | |
dc.subject.mesh | Cell Death | |
dc.subject.mesh | Epithelial Cells | |
dc.subject.mesh | Epithelium | |
dc.subject.mesh | Galectin 3 | |
dc.subject.mesh | Gene Expression Regulation | |
dc.subject.mesh | Genetic Predisposition to Disease | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Inflammation | |
dc.subject.mesh | Interleukin-8 | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Mice, Inbred DBA | |
dc.subject.mesh | Mitochondria | |
dc.subject.mesh | Neutrophils | |
dc.subject.mesh | Pneumonia | |
dc.subject.mesh | Pulmonary Disease, Chronic Obstructive | |
dc.subject.mesh | Smoking | |
dc.subject.mesh | Epithelium | |
dc.subject.mesh | Neutrophils | |
dc.subject.mesh | Mitochondria | |
dc.subject.mesh | Epithelial Cells | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Mice, Inbred DBA | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Pulmonary Disease, Chronic Obstructive | |
dc.subject.mesh | Pneumonia | |
dc.subject.mesh | Genetic Predisposition to Disease | |
dc.subject.mesh | Inflammation | |
dc.subject.mesh | Antimicrobial Cationic Peptides | |
dc.subject.mesh | Galectin 3 | |
dc.subject.mesh | Interleukin-8 | |
dc.subject.mesh | Administration, Intranasal | |
dc.subject.mesh | Smoking | |
dc.subject.mesh | Cell Death | |
dc.subject.mesh | Gene Expression Regulation | |
dc.subject.mesh | Adult | |
dc.subject.mesh | Cathelicidins | |
dc.subject.mesh | Alarmins | |
dc.title | Susceptibility for cigarette smoke-induced DAMP release and DAMP-induced inflammation in COPD. | |
dc.type | Journal Article | |
utslib.citation.volume | 311 | |
utslib.location.activity | United States | |
utslib.for | 0606 Physiology | |
utslib.for | 1116 Medical Physiology | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
pubs.organisational-group | /University of Technology Sydney/Centre for Health Technologies (CHT) | |
utslib.copyright.status | closed_access | * |
dc.date.updated | 2022-07-29T22:24:38Z | |
pubs.issue | 5 | |
pubs.publication-status | Published | |
pubs.volume | 311 | |
utslib.citation.issue | 5 |
Abstract:
Cigarette smoke (CS) exposure is a major risk factor for chronic obstructive pulmonary disease (COPD). We investigated whether CS-induced damage-associated molecular pattern (DAMP) release or DAMP-mediated inflammation contributes to susceptibility for COPD. Samples, including bronchial brushings, were collected from young and old individuals, susceptible and nonsusceptible for the development of COPD, before and after smoking, and used for gene profiling and airway epithelial cell (AEC) culture. AECs were exposed to CS extract (CSE) or specific DAMPs. BALB/cByJ and DBA/2J mice were intranasally exposed to LL-37 and mitochondrial (mt)DAMPs. Functional gene-set enrichment analysis showed that CS significantly increases the airway epithelial gene expression of DAMPs and DAMP receptors in COPD patients. In cultured AECs, we observed that CSE induces necrosis and DAMP release, with specifically higher galectin-3 release from COPD-derived compared with control-derived cells. Galectin-3, LL-37, and mtDAMPs increased CXCL8 secretion in AECs. LL-37 and mtDAMPs induced neutrophilic airway inflammation, exclusively in mice susceptible for CS-induced airway inflammation. Collectively, we show that in airway epithelium from COPD patients, the CS-induced expression of DAMPs and DAMP receptors in vivo and the release of galectin-3 in vitro is exaggerated. Furthermore, our studies indicate that a predisposition to release DAMPs and subsequent induction of inflammation may contribute to the development of COPD.
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