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.
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.
authors.affiliation: Host-Pathogen Translational Research Group, Faculté de Médecine de Lille UDSL-Université Lille Nord de France, Lille, France.
authors.forename: Jean Baptiste
authors.initials: JB
authors.lastname: Mear
authors.forename: Philippe
authors.initials: P
authors.lastname: Gosset
authors.forename: Eric
authors.initials: E
authors.lastname: Kipnis
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Faure
authors.forename: Rodrigue
authors.initials: R
authors.lastname: Dessein
authors.forename: Samir
authors.initials: S
authors.lastname: Jawhara
authors.forename: Chantal
authors.initials: C
authors.lastname: Fradin
authors.forename: Karine
authors.initials: K
authors.lastname: Faure
authors.forename: Daniel
authors.initials: D
authors.lastname: Poulain
authors.forename: Boualem
authors.initials: B
authors.lastname: Sendid
authors.forename: Benoit
authors.initials: B
authors.lastname: Guery
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002176:Candida albicans / Q000276:immunology / Q000502:physiology*; D003713:Dendritic Cells / Q000276:immunology; D004195:Disease Models, Animal; D005434:Flow Cytometry; D007111:Immunity, Cellular / Q000276:immunology; D007113:Immunity, Innate / Q000276:immunology* / Q000502:physiology; D007378:Interleukins / Q000276:immunology* / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology; D055370:Lung Injury / Q000276:immunology / Q000382:microbiology*; D008214:Lymphocytes / Q000276:immunology* / Q000378:metabolism; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D011552:Pseudomonas Infections / Q000276:immunology*; D011550:Pseudomonas aeruginosa / Q000276:immunology*; D000097043:Interleukin-22
chemical_list: D007378:Interleukins; D000097043:Interleukin-22