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Inactivation of the interleukin-22 pathway in the airways of cystic fibrosis patients

Abstract : Interleukin (IL)-22 plays a critical role in regulating the maintenance of the mucosal barrier. As airway epithelial regeneration is abnormal in cystic fibrosis (CF), we investigated IL-22 integrity in CF. We first demonstrated, using Il-22-/- mice, that IL-22 is important to prevent lung damage induced by the CF pathogen Pseudomonas aeruginosa. Next, IL-22 receptor was found normally expressed at the airway epithelial surfaces of CF patients. In wound-healing assays, IL-22-treated CF cultures had higher wound-closure rate than controls, suggesting that IL-22 signaling per se could be functional in a CF context. However, persistence of neutrophil-derived serine-proteases is a major feature of CF airways. Remarkably, IL-22 was found altered in this protease-rich inflammatory microenvironment; the serine protease-3 being the most prone to fully degrade IL-22. Consequently, we suspect an acquired deficiency of the IL-22 pathway in the lungs of CF patients due to IL-22 cleavage by the surrounding neutrophil serine-proteases.
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Contributor : Valerian Dormoy <>
Submitted on : Thursday, July 2, 2020 - 3:05:24 PM
Last modification on : Monday, May 17, 2021 - 2:52:23 PM



Antoine Guillon, Deborah Brea, Emilie Luczka, Virginie Herve, Soujoud Hasanat, et al.. Inactivation of the interleukin-22 pathway in the airways of cystic fibrosis patients. Cytokine, Elsevier, 2019, 113 (1), pp.470-474. ⟨10.1016/j.cyto.2018.10.015⟩. ⟨hal-02448633⟩



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