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

Journal article

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 PAB, Sin DD, Caramori G, Adcock IM, Foster PS, Hansbro PM.
Eur Respir J, vol. 54(1), 2019, p. 1800174

DOI: 10.1183/13993003.00174-2018

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APA Click to copy
MR, S., MW, P., P, C., A, P., S, P., Y, G., … PM., H. (2019). IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis. Eur Respir J, 54(1), 1800174. https://doi.org/10.1183/13993003.00174-2018

Chicago/Turabian Click to copy
MR, Starkey, Plank MW, Casolari P, Papi A, Pavlidis S, Guo Y, Cameron GJM, et al. “IL-22 and Its Receptors Are Increased in Human and Experimental COPD and Contribute to Pathogenesis.” Eur Respir J 54, no. 1 (2019): 1800174.

MLA Click to copy
MR, Starkey, et al. “IL-22 and Its Receptors Are Increased in Human and Experimental COPD and Contribute to Pathogenesis.” Eur Respir J, vol. 54, no. 1, 2019, p. 1800174, doi:10.1183/13993003.00174-2018.

BibTeX Click to copy

@article{starkey2019a,
  title = {IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis},
  year = {2019},
  issue = {1},
  journal = {Eur Respir J},
  pages = {1800174},
  volume = {54},
  doi = {10.1183/13993003.00174-2018},
  author = {MR, Starkey and MW, Plank and P, Casolari and A, Papi and S, Pavlidis and Y, Guo and GJM, Cameron and TJ, Haw and A, Tam and M, Obiedat and C, Donovan and NG, Hansbro and DH, Nguyen and PM, Nair and RY, Kim and JC, Horvat and GE, Kaiko and SK, Durum and PAB, Wark and DD, Sin and G, Caramori and IM, Adcock and PS, Foster and PM., Hansbro}
}

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.

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https://doi.org/10.1183/13993003.00174-2018