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
Infect Immun
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
Volume
82
Number
1
Pages
306-15
Language
english
Notes
Mear, Jean Baptiste
Gosset, Philippe
Kipnis, Eric
Faure, Emmanuel
Dessein, Rodrigue
Jawhara, Samir
Fradin, Chantal
Faure, Karine
Poulain, Daniel
Sendid, Boualem
Guery, Benoit
eng
Infect Immun. 2014 Jan;82(1):306-15. doi: 10.1128/IAI.01085-13. Epub 2013 Oct 28.
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/*physiology, Dendritic Cells/immunology, Disease Models, Animal, Flow Cytometry, Immunity, Cellular/immunology, Immunity, Innate/*immunology/physiology, Interleukins/*immunology/metabolism, Killer Cells, Natural/immunology, Lung Injury/immunology/*microbiology, Lymphocytes/*immunology/metabolism, Macrophages/immunology, Mice, Mice, Inbred C57BL, Pseudomonas Infections/*immunology, Pseudomonas aeruginosa/*immunology
Pubmed
Create date
29/04/2021 10:59
Last modification date
30/04/2021 6:38
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