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IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis

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Title: IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis
Authors: Starkey, MR
Plank, MW
Casolari, P
Papi, A
Pavlidis, S
Guo, Y
Cameron, GJM
Haw, TJ
Tam, A
Obiedat, M
Donovan, C
Hansbro, NG
Nguyen, DH
Nair, PM
Kim, RY
Horvat, JC
Kaiko, GE
Durum, SK
Wark, PA
Sin, DD
Caramori, G
Adcock, IM
Foster, PS
Hansbro, PM
Item Type: Journal Article
Abstract: Chronic obstructive pulmonary disease (COPD) is the third leading cause of morbidity and death globally. The lack of effective treatments results from an incomplete understanding of the underlying mechanisms driving COPD pathogenesis. Interleukin (IL)-22 has been implicated in airway inflammation and is increased in COPD patients. However, its roles in the pathogenesis of COPD is poorly understood. Here, we investigated the role of IL-22 in human COPD and in cigarette smoke (CS)-induced experimental COPD. IL-22 and IL-22 receptor mRNA expression and protein levels were increased in COPD patients compared to healthy smoking or non-smoking controls. IL-22 and IL-22 receptor levels were increased in the lungs of mice with experimental COPD compared to controls and the cellular source of IL-22 included CD4+ T-helper cells, γδ T-cells, natural killer T-cells and group 3 innate lymphoid cells. CS-induced pulmonary neutrophils were reduced in IL-22-deficient (Il22−/−) mice. CS-induced airway remodelling and emphysema-like alveolar enlargement did not occur in Il22−/− mice. Il22−/− mice had improved lung function in terms of airway resistance, total lung capacity, inspiratory capacity, forced vital capacity and compliance. These data highlight important roles for IL-22 and its receptors in human COPD and CS-induced experimental COPD.
Issue Date: 1-Jul-2019
Date of Acceptance: 19-Apr-2019
URI: http://hdl.handle.net/10044/1/83993
DOI: 10.1183/13993003.00174-2018
ISSN: 0903-1936
Publisher: European Respiratory Society
Start Page: 1
End Page: 14
Journal / Book Title: European Respiratory Journal
Volume: 54
Issue: 1
Copyright Statement: © ERS 2019
Sponsor/Funder: Wellcome Trust
Funder's Grant Number: 093080/Z/10/Z
Keywords: Science & Technology
Life Sciences & Biomedicine
Respiratory System
OBSTRUCTIVE PULMONARY-DISEASE
APOPTOSIS-INDUCING LIGAND
CIGARETTE-SMOKE
RESPIRATORY-INFECTION
AIRWAY EPITHELIUM
ANIMAL-MODELS
EXPRESSION
RESPONSES
FEATURES
ASTHMA
Airway Remodeling
Airway Resistance
Animals
Emphysema
Female
Humans
Immunity, Innate
Interleukins
Lymphocytes
Mice
Mice, Inbred C57BL
Mice, Knockout
Pulmonary Disease, Chronic Obstructive
Receptors, Interleukin
Smoke
Tobacco Products
Lymphocytes
Animals
Mice, Inbred C57BL
Mice, Knockout
Humans
Mice
Pulmonary Disease, Chronic Obstructive
Emphysema
Receptors, Interleukin
Interleukins
Airway Resistance
Smoke
Female
Immunity, Innate
Airway Remodeling
Tobacco Products
Science & Technology
Life Sciences & Biomedicine
Respiratory System
OBSTRUCTIVE PULMONARY-DISEASE
APOPTOSIS-INDUCING LIGAND
CIGARETTE-SMOKE
RESPIRATORY-INFECTION
AIRWAY EPITHELIUM
ANIMAL-MODELS
EXPRESSION
RESPONSES
FEATURES
ASTHMA
11 Medical and Health Sciences
Respiratory System
Publication Status: Published
Open Access location: https://erj.ersjournals.com/content/54/1/1800174
Article Number: ARTN 1800174
Online Publication Date: 2019-07-18
Appears in Collections:National Heart and Lung Institute
Airway Disease