Persistence of candida albicans in the oral mucosa induces a curbed inflammatory host response that is independent of immunosuppression

Autor: Katharina Littringer, Van Du T. Tran, Nicole Joller, Dominique Sanglard, Florian R. Kirchner, Simon Altmeier, Salomé LeibundGut-Landmann, Franziska Schönherr, Marco Pagni, Christina Lemberg
Přispěvatelé: University of Zurich, LeibundGut-Landmann, Salomé
Jazyk: angličtina
Rok vydání: 2019
Předmět:
0301 basic medicine
medicine.medical_treatment
10263 Institute of Experimental Immunology
T-Lymphocytes
Regulatory
regulatory T cells
Mice
0302 clinical medicine
Candidiasis
Oral
Candida albicans
IL-10
IL-17
immune regulation
oropharyngeal candidiasis
persistence
Immunology and Allergy
Oral mucosa
Original Research
Mice
Knockout
Virulence
Immunosuppression
Corpus albicans
Interleukin 10
medicine.anatomical_structure
Host-Pathogen Interactions
2723 Immunology and Allergy
Cytokines
10244 Institute of Virology
lcsh:Immunologic diseases. Allergy
Immunology
Biology
Oropharyngeal Candidiasis
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
Mouth Mucosa/immunology
Mouth Mucosa/microbiology
Species Specificity
T-Lymphocytes
Regulatory/immunology
T-Lymphocytes
Regulatory/metabolism
Virulence/genetics
Microbiology
03 medical and health sciences
Immune system
Immunity
medicine
2403 Immunology
Mouth Mucosa
IL
biology.organism_classification
030104 developmental biology
570 Life sciences
biology
lcsh:RC581-607
030215 immunology
Zdroj: Frontiers in Immunology
Frontiers in Immunology, Vol 10 (2019)
Frontiers in immunology, vol. 10, pp. 330
Popis: 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.
Databáze: OpenAIRE
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