Titre
Candida albicans airway exposure primes the lung innate immune response against Pseudomonas aeruginosa infection through innate lymphoid cell recruitment and interleukin-22-associated mucosal response.
Type
article
Institution
Externe
Périodique
Auteur(s)
Mear, J.B.
Auteure/Auteur
Gosset, P.
Auteure/Auteur
Kipnis, E.
Auteure/Auteur
Faure, E.
Auteure/Auteur
Dessein, R.
Auteure/Auteur
Jawhara, S.
Auteure/Auteur
Fradin, C.
Auteure/Auteur
Faure, K.
Auteure/Auteur
Poulain, D.
Auteure/Auteur
Sendid, B.
Auteure/Auteur
Guery, B.
Auteure/Auteur
Liens vers les personnes
ISSN
1098-5522
Statut éditorial
Publié
Date de publication
2014-01
Volume
82
Numéro
1
Première page
306
Dernière page/numéro d’article
315
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Publication Status: ppublish
Résumé
Pseudomonas aeruginosa and Candida albicans are two pathogens frequently encountered in the intensive care unit microbial community. We have demonstrated that C. albicans airway exposure protected against P. aeruginosa-induced lung injury. The goal of the present study was to characterize the cellular and molecular mechanisms associated with C. albicans-induced protection. Airway exposure by C. albicans led to the recruitment and activation of natural killer cells, innate lymphoid cells (ILCs), macrophages, and dendritic cells. This recruitment was associated with the secretion of interleukin-22 (IL-22), whose neutralization abolished C. albicans-induced protection. We identified, by flow cytometry, ILCs as the only cellular source of IL-22. Depletion of ILCs by anti-CD90.2 antibodies was associated with a decreased IL-22 secretion and impaired survival after P. aeruginosa challenge. Our results demonstrate that the production of IL-22, mainly by ILCs, is a major and inducible step in protection against P. aeruginosa-induced lung injury. This cytokine may represent a clinical target in Pseudomonas aeruginosa-induced lung injury.
Sujets
PID Serval
serval:BIB_BCA98D475C71
PMID
Open Access
Oui
Date de création
2021-04-29T08:59:33.330Z
Date de création dans IRIS
2025-05-20T21:13:46Z