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IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis.
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- Author(s): Starkey MR;Starkey MR; Plank MW; Plank MW; Casolari P; Casolari P; Papi A; Papi A; Pavlidis S; Pavlidis S; Guo Y; Guo Y; Cameron GJM; Cameron GJM; Haw TJ; Haw TJ; Tam A; Tam A; Tam A; Obiedat M; Obiedat M; Obiedat M; Donovan C; Donovan C; Hansbro NG; Hansbro NG; Hansbro NG; Hansbro NG; Nguyen DH; Nguyen DH; Nair PM; Nair PM; Kim RY; Kim RY; Horvat JC; Horvat JC; Kaiko GE; Kaiko GE; Durum SK; Durum SK; Wark PA; Wark PA; Sin DD; Sin DD; Sin DD; Caramori G; Caramori G; Adcock IM; Adcock IM; Foster PS; Foster PS; Hansbro PM; Hansbro PM; Hansbro PM; Hansbro PM
- Source:
The European respiratory journal [Eur Respir J] 2019 Jul 18; Vol. 54 (1). Date of Electronic Publication: 2019 Jul 18 (Print Publication: 2019).- Publication Type:
Journal Article; Research Support, Non-U.S. Gov't- Language:
English - Source:
- Additional Information
- Source: Publisher: European Respiratory Society Country of Publication: England NLM ID: 8803460 Publication Model: Electronic-Print Cited Medium: Internet ISSN: 1399-3003 (Electronic) Linking ISSN: 09031936 NLM ISO Abbreviation: Eur Respir J Subsets: MEDLINE
- Publication Information: Publication: Sheffield, United Kingdom : European Respiratory Society
Original Publication: Copenhagen : Published jointly by the Society and Munksgaard, 1988- - Subject Terms: Emphysema/*etiology ; Interleukins/*physiology ; Pulmonary Disease, Chronic Obstructive/*pathology ; Receptors, Interleukin/*physiology; Airway Remodeling ; Airway Resistance ; Animals ; Emphysema/pathology ; Female ; Humans ; Immunity, Innate ; Lymphocytes/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pulmonary Disease, Chronic Obstructive/chemically induced ; Pulmonary Disease, Chronic Obstructive/metabolism ; Smoke/adverse effects ; Tobacco Products ; Interleukin-22
- 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.
Competing Interests: Conflict of interest: M.R. Starkey has nothing to disclose. Conflict of interest: M.W. Plank is a full-time employee of GlaxoSmithKline. Conflict of interest: P. Casolari has nothing to disclose. Conflict of interest: A. Papi reports board membership, consultancy, payment for lectures, grants for research and travel expenses reimbursement from Chiesi, AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, Mundipharma and TEVA, payment for lectures and travel expenses reimbursement from Menarini, Novartis, Zambon and Sanofi, outside the submitted work. Conflict of interest: S. Pavlidis has nothing to disclose. Conflict of interest: Y Guo has nothing to disclose. Conflict of interest: G.J.M. Cameron has nothing to disclose. Conflict of interest: T.J. Haw has nothing to disclose. Conflict of interest: A. Tam has nothing to disclose. Conflict of interest: M. Obeidat has nothing to disclose. Conflict of interest: C. Donovan has nothing to disclose. Conflict of interest: N.G. Hansbro has nothing to disclose. Conflict of interest: D.H. Nguyen has nothing to disclose. Conflict of interest: P.M. Nair has nothing to disclose. Conflict of interest: R.Y. Kim has nothing to disclose. Conflict of interest: J.C. Horvat has nothing to disclose. Conflict of interest: G.E. Kaiko has nothing to disclose. Conflict of interest: S.K. Durum has nothing to disclose. Conflict of interest: P.A. Wark has nothing to disclose. Conflict of interest: D.D. Sin reports grants from Merck, personal fees for advisory board work from Sanofi-Aventis and Regeneron, grants and personal fees from Boehringer Ingelheim, grants and personal fees for lecturing and advisory board work from AstraZeneca, personal fees for lecturing and advisory board work from Novartis, outside the submitted work. Conflict of interest: G. Caramori has nothing to disclose. Conflict of interest: I.M. Adcock has nothing to disclose. Conflict of interest: P.S. Foster has nothing to disclose. Conflict of interest: P.M. Hansbro reports funding/consultancies from Pharmaxis, AstraZeneca, Sanofi, Pharmakea, Ausbio, and Allakos outside the submitted work.
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- Accession Number: 0 (Interleukins)
0 (Receptors, Interleukin)
0 (Smoke)
0 (interleukin-22 receptor) - Publication Date: Date Created: 20190615 Date Completed: 20200915 Latest Revision: 20231213
- Publication Date: 20240628
- Accession Number: PMC8132110
- Accession Number: 10.1183/13993003.00174-2018
- Accession Number: 31196943
- Source:
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