Inactivation of the interleukin-22 pathway ...
Document type :
Article dans une revue scientifique
PMID :
Permalink :
Title :
Inactivation of the interleukin-22 pathway in the airways of cystic fibrosis patients
Author(s) :
Guillon, Antoine [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Brea, Deborah [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Luczka, Emilie [Auteur]
Pathologies Pulmonaires et Plasticité Cellulaire - UMR-S 1250 [P3CELL]
Herve, Virginie [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Hasanat, Soujoud [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Thorey, Camille [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Pérez-Cruz, Magdiel [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Hordeaux, Juliette [Auteur]
Mankikian, Julie [Auteur]
Centre Hospitalier Régional Universitaire de Tours [CHRU Tours]
Gosset, Philippe [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Coraux, Christelle [Auteur]
Pathologies Pulmonaires et Plasticité Cellulaire - UMR-S 1250 [P3CELL]
Si-Tahar, Mustapha [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Brea, Deborah [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Luczka, Emilie [Auteur]
Pathologies Pulmonaires et Plasticité Cellulaire - UMR-S 1250 [P3CELL]
Herve, Virginie [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Hasanat, Soujoud [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Thorey, Camille [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Pérez-Cruz, Magdiel [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Hordeaux, Juliette [Auteur]
Mankikian, Julie [Auteur]
Centre Hospitalier Régional Universitaire de Tours [CHRU Tours]
Gosset, Philippe [Auteur]

Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Coraux, Christelle [Auteur]
Pathologies Pulmonaires et Plasticité Cellulaire - UMR-S 1250 [P3CELL]
Si-Tahar, Mustapha [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Université de Tours [UT]
Journal title :
Cytokine
Pages :
470-474
Publisher :
Elsevier
Publication date :
2019-01
ISSN :
1043-4666
English keyword(s) :
Cystic fibrosis
IL-22
Neutrophil proteases
Pseudomonas aeruginosa
Respiratory infection
IL-22
Neutrophil proteases
Pseudomonas aeruginosa
Respiratory infection
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
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 ...
Show more >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.Show less >
Show more >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.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Source :
Submission date :
2022-03-13T02:30:49Z
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