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.

Details

Serval ID
serval:BIB_BCA98D475C71
Type
Article: article from journal or magazin.
Collection
Publications
Title
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.
Journal
Infection and immunity
Author(s)
Mear J.B., Gosset P., Kipnis E., Faure E., Dessein R., Jawhara S., Fradin C., Faure K., Poulain D., Sendid B., Guery B.
ISSN
1098-5522 (Electronic)
ISSN-L
0019-9567
Publication state
Published
Issued date
01/2014
Peer-reviewed
Oui
Volume
82
Number
1
Pages
306-315
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Abstract
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.
Keywords
Analysis of Variance, Animals, Candida albicans/immunology, Candida albicans/physiology, Dendritic Cells/immunology, Disease Models, Animal, Flow Cytometry, Immunity, Cellular/immunology, Immunity, Innate/immunology, Immunity, Innate/physiology, Interleukins/immunology, Interleukins/metabolism, Killer Cells, Natural/immunology, Lung Injury/immunology, Lung Injury/microbiology, Lymphocytes/immunology, Lymphocytes/metabolism, Macrophages/immunology, Mice, Mice, Inbred C57BL, Pseudomonas Infections/immunology, Pseudomonas aeruginosa/immunology
Pubmed
Web of science
Open Access
Yes
Create date
29/04/2021 10:59
Last modification date
17/07/2023 13:04
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