A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease.

Haw, TJ; Starkey, MR; Nair, PM; Pavlidis, S; Liu, G; Nguyen, DH; Hsu, AC; Hanish, I; Kim, RY; Collison, AM; Inman, MD; Wark, PA; Foster, PS; Knight, DA; Mattes, J; Yagita, H; Adcock, IM; Horvat, JC; Hansbro, PM

A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease.

Haw, TJ Starkey, MR Nair, PM Pavlidis, S Liu, G

Nguyen, DH Hsu, AC Hanish, I Kim, RY Collison, AM Inman, MD Wark, PA Foster, PS Knight, DA Mattes, J Yagita, H Adcock, IM Horvat, JC Hansbro, PM

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Publisher:: SPRINGERNATURE
Publication Type:: Journal Article
Citation:: Mucosal immunology, 2016, 9, (4), pp. 859-872
Issue Date:: 2016-07

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Field	Value	Language
dc.contributor.author	Haw, TJ
dc.contributor.author	Starkey, MR
dc.contributor.author	Nair, PM
dc.contributor.author	Pavlidis, S
dc.contributor.author	Liu, G https://orcid.org/0000-0002-0489-2638
dc.contributor.author	Nguyen, DH
dc.contributor.author	Hsu, AC
dc.contributor.author	Hanish, I
dc.contributor.author	Kim, RY
dc.contributor.author	Collison, AM
dc.contributor.author	Inman, MD
dc.contributor.author	Wark, PA
dc.contributor.author	Foster, PS
dc.contributor.author	Knight, DA
dc.contributor.author	Mattes, J
dc.contributor.author	Yagita, H
dc.contributor.author	Adcock, IM
dc.contributor.author	Horvat, JC
dc.contributor.author	Hansbro, PM
dc.date.accessioned	2021-01-04T23:08:53Z
dc.date.available	2015-09-18
dc.date.available	2021-01-04T23:08:53Z
dc.date.issued	2016-07
dc.identifier.citation	Mucosal immunology, 2016, 9, (4), pp. 859-872
dc.identifier.issn	1933-0219
dc.identifier.issn	1935-3456
dc.identifier.uri	http://hdl.handle.net/10453/145074
dc.description.abstract	Chronic obstructive pulmonary disease (COPD) is a life-threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective therapies is impaired by a lack of understanding of the underlining mechanisms. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine with inflammatory and apoptotic properties. We interrogated a mouse model of CS-induced experimental COPD and human tissues to identify a novel role for TRAIL in COPD pathogenesis. CS exposure of wild-type mice increased TRAIL and its receptor messenger RNA (mRNA) expression and protein levels, as well as the number of TRAIL(+)CD11b(+) monocytes in the lung. TRAIL and its receptor mRNA were also increased in human COPD. CS-exposed TRAIL-deficient mice had decreased pulmonary inflammation, pro-inflammatory mediators, emphysema-like alveolar enlargement, and improved lung function. TRAIL-deficient mice also developed spontaneous small airway changes with increased epithelial cell thickness and collagen deposition, independent of CS exposure. Importantly, therapeutic neutralization of TRAIL, after the establishment of early-stage experimental COPD, reduced pulmonary inflammation, emphysema-like alveolar enlargement, and small airway changes. These data provide further evidence for TRAIL being a pivotal inflammatory factor in respiratory diseases, and the first preclinical evidence to suggest that therapeutic agents that target TRAIL may be effective in COPD therapy.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	SPRINGERNATURE
dc.relation.ispartof	Mucosal immunology
dc.relation.isbasedon	10.1038/mi.2015.111
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject	06 Biological Sciences, 11 Medical and Health Sciences
dc.subject.classification	Immunology
dc.subject.mesh	Lung
dc.subject.mesh	Respiratory Mucosa
dc.subject.mesh	Monocytes
dc.subject.mesh	Animals
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	Mice, Knockout
dc.subject.mesh	Humans
dc.subject.mesh	Mice
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Inflammation
dc.subject.mesh	RNA, Messenger
dc.subject.mesh	Inflammation Mediators
dc.subject.mesh	Smoking
dc.subject.mesh	Apoptosis
dc.subject.mesh	Up-Regulation
dc.subject.mesh	Female
dc.subject.mesh	TNF-Related Apoptosis-Inducing Ligand
dc.subject.mesh	Animals
dc.subject.mesh	Apoptosis
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Female
dc.subject.mesh	Humans
dc.subject.mesh	Inflammation
dc.subject.mesh	Inflammation Mediators
dc.subject.mesh	Lung
dc.subject.mesh	Mice
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	Mice, Knockout
dc.subject.mesh	Monocytes
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	RNA, Messenger
dc.subject.mesh	Respiratory Mucosa
dc.subject.mesh	Smoking
dc.subject.mesh	TNF-Related Apoptosis-Inducing Ligand
dc.subject.mesh	Up-Regulation
dc.title	A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease.
dc.type	Journal Article
utslib.citation.volume	9
utslib.location.activity	United States
utslib.for	06 Biological Sciences
utslib.for	11 Medical and Health Sciences
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
utslib.copyright.status	closed_access	*
dc.date.updated	2021-01-04T23:08:45Z
pubs.issue	4
pubs.publication-status	Published
pubs.volume	9
utslib.citation.issue	4

Abstract:

Chronic obstructive pulmonary disease (COPD) is a life-threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective therapies is impaired by a lack of understanding of the underlining mechanisms. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine with inflammatory and apoptotic properties. We interrogated a mouse model of CS-induced experimental COPD and human tissues to identify a novel role for TRAIL in COPD pathogenesis. CS exposure of wild-type mice increased TRAIL and its receptor messenger RNA (mRNA) expression and protein levels, as well as the number of TRAIL(+)CD11b(+) monocytes in the lung. TRAIL and its receptor mRNA were also increased in human COPD. CS-exposed TRAIL-deficient mice had decreased pulmonary inflammation, pro-inflammatory mediators, emphysema-like alveolar enlargement, and improved lung function. TRAIL-deficient mice also developed spontaneous small airway changes with increased epithelial cell thickness and collagen deposition, independent of CS exposure. Importantly, therapeutic neutralization of TRAIL, after the establishment of early-stage experimental COPD, reduced pulmonary inflammation, emphysema-like alveolar enlargement, and small airway changes. These data provide further evidence for TRAIL being a pivotal inflammatory factor in respiratory diseases, and the first preclinical evidence to suggest that therapeutic agents that target TRAIL may be effective in COPD therapy.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/145074