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IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis
File | Description | Size | Format | |
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Accepted version IL-22 COPD ERJ.pdf | Accepted version | 5.04 MB | Adobe PDF | View/Open |
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 |