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IL-22 exacerbates weight loss in a murine model of chronic pulmonary Pseudomonas aeruginosa infection

Lookup NU author(s): Professor Christopher WardORCiD, Dr Malcolm BrodlieORCiD

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).

Abstract

BACKGROUND:Interleukin (IL)-22 is a critical mediator of mucosal immunity and tissue regeneration, protecting against a number of respiratory pathogens. Whether IL-22 confers protection against chronic Pseudomonas aeruginosa (PA) infection in cystic fibrosis (CF) is unknown.METHODS:Explanted CF lungs were examined for IL-22 production and immune-localization. A murine model of persistent pulmonary PA infection was used to examine production of IL-22 following infective challenge. The role of IL-22 was examined using IL-22 knockout (KO) animals.RESULTS:IL-22 is produced within the adult CF lung and localizes to the airway epithelium. IL-22 is produced by murine pulmonary lymph node cells following lung infection. The absence of IL-22 resulted in no significant difference in acute mortality, bacterial burden, chronic infection rates, histological changes or neutrophilic inflammation in the chronic PA infection model. However, IL-22 KO animals lost less weight following infection.CONCLUSION:IL-22 is produced in the CF lung and in response to PA infection yet is dispensable in protection against chronic pulmonary P. aeruginosa infection in a murine model. However, we identified a novel role for the cytokine in promoting infection-related weight-loss, a significant prognostic factor in the CF population.

Publication metadata

Author(s): Bayes HK, Ritchie ND, Ward C, Corris PA, Brodlie M, Evans TJ

Publication type: Article

Publication status: Published

Journal: Journal of Cystic Fibrosis

Year: 2016

Volume: 15

Issue: 6

Pages: 759–768

Print publication date: 01/11/2016

Online publication date: 01/07/2016

Acceptance date: 15/06/2016

Date deposited: 26/07/2016

ISSN (print): 1569-1993

ISSN (electronic): 1873-5010

Publisher: Elsevier

URL: http://dx.doi.org/10.1016/j.jcf.2016.06.008

DOI: 10.1016/j.jcf.2016.06.008

PubMed id: 27375092

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