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Pseudomonas aeruginosa andCandida albicans are two pathogens frequently encountered in the intensive care unit microbial community. We have demonstrated thatC. albicans airway exposure protected againstP. aeruginosa -induced lung injury. The goal of the present study was to characterize the cellular and molecular mechanisms associated withC. albicans -induced protection. Airway exposure byC. 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 abolishedC. 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 afterP. aeruginosa challenge. Our results demonstrate that the production of IL-22, mainly by ILCs, is a major and inducible step in protection againstP. aeruginosa -induced lung injury. This cytokine may represent a clinical target inPseudomonas aeruginosa -induced lung injury.

infection and immunity

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