Pseudomonas aeruginosa proteolytically ...
Type de document :
Article dans une revue scientifique
PMID :
URL permanente :
Titre :
Pseudomonas aeruginosa proteolytically alters the interleukin 22-dependent lung mucosal defense
Auteur(s) :
Guillon, Antoine [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Centre Hospitalier Régional Universitaire de Tours [CHRU Tours]
Brea, Deborah [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Morello, Eric [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Tang, Aihua [Auteur]
University of Mississippi Medical Center [UMMC]
Jouan, Youenn [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Centre Hospitalier Régional Universitaire de Tours [CHRU Tours]
Ramphal, Reuben [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Korkmaz, Brice [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Perez-Cruz, Magdiel [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Trottein, Francois [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
O'Callaghan, Richard [Auteur]
University of Mississippi Medical Center [UMMC]
Gosset, Philippe [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Si-Tahar, Mustapha [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Centre Hospitalier Régional Universitaire de Tours [CHRU Tours]
Brea, Deborah [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Morello, Eric [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Tang, Aihua [Auteur]
University of Mississippi Medical Center [UMMC]
Jouan, Youenn [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Centre Hospitalier Régional Universitaire de Tours [CHRU Tours]
Ramphal, Reuben [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Korkmaz, Brice [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Perez-Cruz, Magdiel [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Trottein, Francois [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
O'Callaghan, Richard [Auteur]
University of Mississippi Medical Center [UMMC]
Gosset, Philippe [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Si-Tahar, Mustapha [Auteur]
Centre d’Etude des Pathologies Respiratoires (CEPR), UMR 1100 [CEPR]
Titre de la revue :
Virulence
Pagination :
810-820
Éditeur :
Taylor & Francis
Date de publication :
2016-10-28
ISSN :
2150-5594
Mot(s)-clé(s) en anglais :
Pseudomonas aeruginosa
infection
interleukin 22
lung
proteases
infection
interleukin 22
lung
proteases
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
The IL-22 signaling pathway is critical for regulating mucosal defense and limiting bacterial dissemination. IL-22 is unusual among interleukins because it does not directly regulate the function of conventional immune ...
Lire la suite >The IL-22 signaling pathway is critical for regulating mucosal defense and limiting bacterial dissemination. IL-22 is unusual among interleukins because it does not directly regulate the function of conventional immune cells, but instead targets cells at outer body barriers, such as respiratory epithelial cells. Consequently, IL-22 signaling participates in the maintenance of the lung mucosal barrier by controlling cell proliferation and tissue repair, and enhancing the production of specific chemokines and anti-microbial peptides. Pseudomonas aeruginosa is a major pathogen of ventilator-associated pneumonia and causes considerable lung tissue damage. A feature underlying the pathogenicity of this bacterium is its capacity to persist and develop in the host, particularly in the clinical context of nosocomial lung infections. We aimed to investigate the ability of P. auruginosa to disrupt immune-epithelial cells cross-talk. We found that P. aeruginosa escapes the host mucosal defenses by degrading IL-22, leading to severe inhibition of IL-22-mediated immune responses. We demonstrated in vitro that, protease IV, a type 2 secretion system-dependent serine protease, is responsible for the degradation of IL-22 by P. aeruginosa. Moreover, the major anti-proteases molecules present in the lungs were unable to inhibit protease IV enzymatic activity. In addition, tracheal aspirates of patients infected by P. aeruginosa contain protease IV activity which further results in IL-22 degradation. This so far undescribed cleavage of IL-22 by a bacterial protease is likely to be an immune-evasion strategy that contributes to P. aeruginosa-triggered respiratory infections.Lire moins >
Lire la suite >The IL-22 signaling pathway is critical for regulating mucosal defense and limiting bacterial dissemination. IL-22 is unusual among interleukins because it does not directly regulate the function of conventional immune cells, but instead targets cells at outer body barriers, such as respiratory epithelial cells. Consequently, IL-22 signaling participates in the maintenance of the lung mucosal barrier by controlling cell proliferation and tissue repair, and enhancing the production of specific chemokines and anti-microbial peptides. Pseudomonas aeruginosa is a major pathogen of ventilator-associated pneumonia and causes considerable lung tissue damage. A feature underlying the pathogenicity of this bacterium is its capacity to persist and develop in the host, particularly in the clinical context of nosocomial lung infections. We aimed to investigate the ability of P. auruginosa to disrupt immune-epithelial cells cross-talk. We found that P. aeruginosa escapes the host mucosal defenses by degrading IL-22, leading to severe inhibition of IL-22-mediated immune responses. We demonstrated in vitro that, protease IV, a type 2 secretion system-dependent serine protease, is responsible for the degradation of IL-22 by P. aeruginosa. Moreover, the major anti-proteases molecules present in the lungs were unable to inhibit protease IV enzymatic activity. In addition, tracheal aspirates of patients infected by P. aeruginosa contain protease IV activity which further results in IL-22 degradation. This so far undescribed cleavage of IL-22 by a bacterial protease is likely to be an immune-evasion strategy that contributes to P. aeruginosa-triggered respiratory infections.Lire moins >
Langue :
Anglais
Comité de lecture :
Oui
Audience :
Internationale
Vulgarisation :
Non
Source :
Date de dépôt :
2022-01-23T02:31:47Z