Persistence of Candida albicans in the Oral Mucosa Induces a Curbed Inflammatory Host Response That Is Independent of Immunosuppression.

Details

Serval ID
serval:BIB_D64DED349677
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Persistence of Candida albicans in the Oral Mucosa Induces a Curbed Inflammatory Host Response That Is Independent of Immunosuppression.
Journal
Frontiers in immunology
Author(s)
Kirchner F.R., Littringer K., Altmeier S., Tran VDT, Schönherr F., Lemberg C., Pagni M., Sanglard D., Joller N., LeibundGut-Landmann S.
ISSN
1664-3224 (Electronic)
ISSN-L
1664-3224
Publication state
Published
Issued date
2019
Peer-reviewed
Oui
Volume
10
Pages
330
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Abstract
Controlled immune activation in response to commensal microbes is critical for the maintenance of stable colonization and prevention of microbial overgrowth on epithelial surfaces. Our understanding of the host mechanisms that regulate bacterial commensalism has increased substantially, however, much less data exist regarding host responses to members of the fungal microbiota on colonized surfaces. Using a murine model of oropharyngeal candidiasis, we have recently shown that differences in immune activation in response to diverse natural isolates of Candida albicans are associated with different outcomes of the host-fungal interaction. Here we applied a genome-wide transcriptomic approach to show that rapid induction of a strong inflammatory response characterized by neutrophil-associated genes upon C. albicans colonization inversely correlated with the ability of the fungus to persist in the oral mucosa. Surprisingly, persistent fungal isolates showed no signs of a compensatory regulatory immune response. By combining RNA-seq data, genetic mouse models, and co-infection experiments, we show that attenuation of the inflammatory response at the onset of infection with a persistent isolate is not a consequence of enhanced immunosuppression. Importantly, depletion of regulatory T cells or deletion of the immunoregulatory cytokine IL-10 did not alter host-protective type 17 immunity nor did it impair fungal survival in the oral mucosa, indicating that persistence of C. albicans in the oral mucosa is not a consequence of suppressed antifungal immunity.
Keywords
Animals, Candida albicans/immunology, Candidiasis, Oral/immunology, Candidiasis, Oral/microbiology, Cytokines/biosynthesis, Disease Models, Animal, Gene Expression Profiling, Gene Expression Regulation, Host-Pathogen Interactions/genetics, Host-Pathogen Interactions/immunology, Immune Tolerance, Immunomodulation, Mice, Mice, Knockout, Mouth Mucosa/immunology, Mouth Mucosa/microbiology, Species Specificity, T-Lymphocytes, Regulatory/immunology, T-Lymphocytes, Regulatory/metabolism, Virulence/genetics, Candida albicans, IL-10, IL-17, immune regulation, oropharyngeal candidiasis, persistence, regulatory T cells
Pubmed
Web of science
Open Access
Yes
Create date
17/03/2019 16:52
Last modification date
25/07/2020 5:19
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