The intraspecies diversity of C. albicans triggers qualitatively and temporally distinct host responses that determine the balance between commensalism and ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-02-08

AUTHORS

F A Schönherr, F Sparber, F R Kirchner, E Guiducci, K Trautwein-Weidner, A Gladiator, N Sertour, U Hetzel, G T T Le, N Pavelka, C d'Enfert, M-E Bougnoux, C F Corti, S LeibundGut-Landmann

ABSTRACT

The host immune status is critical for preventing opportunistic infections with Candida albicans. Whether the natural fungal diversity that exists between C. albicans isolates also influences disease development remains unclear. Here, we used an experimental model of oral infection to probe the host response to diverse C. albicans isolates in vivo and found dramatic differences in their ability to persist in the oral mucosa, which inversely correlated with the degree and kinetics of immune activation in the host. Strikingly, the requirement of interleukin (IL)-17 signaling for fungal control was conserved between isolates, including isolates with delayed induction of IL-17. This underscores the relevance of IL-17 immunity in mucosal defense against C. albicans. In contrast, the accumulation of neutrophils and induction of inflammation in the infected tissue was strictly strain dependent. The dichotomy of the inflammatory neutrophil response was linked to the capacity of fungal strains to cause cellular damage and release of alarmins from the epithelium. The epithelium thus translates differences in the fungus into qualitatively distinct host responses. Altogether, this study provides a comprehensive understanding of the antifungal response in the oral mucosa and demonstrates the relevance of evaluating intraspecies differences for the outcome of fungal–host interactions in vivo. More... »

PAGES

1335-1350

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/mi.2017.2

DOI

http://dx.doi.org/10.1038/mi.2017.2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1083733670

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28176789


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32 schema:description The host immune status is critical for preventing opportunistic infections with Candida albicans. Whether the natural fungal diversity that exists between C. albicans isolates also influences disease development remains unclear. Here, we used an experimental model of oral infection to probe the host response to diverse C. albicans isolates in vivo and found dramatic differences in their ability to persist in the oral mucosa, which inversely correlated with the degree and kinetics of immune activation in the host. Strikingly, the requirement of interleukin (IL)-17 signaling for fungal control was conserved between isolates, including isolates with delayed induction of IL-17. This underscores the relevance of IL-17 immunity in mucosal defense against C. albicans. In contrast, the accumulation of neutrophils and induction of inflammation in the infected tissue was strictly strain dependent. The dichotomy of the inflammatory neutrophil response was linked to the capacity of fungal strains to cause cellular damage and release of alarmins from the epithelium. The epithelium thus translates differences in the fungus into qualitatively distinct host responses. Altogether, this study provides a comprehensive understanding of the antifungal response in the oral mucosa and demonstrates the relevance of evaluating intraspecies differences for the outcome of fungal–host interactions in vivo.
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39 Candida albicans
40 IL-17
41 IL-17 immunity
42 ability
43 accumulation
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45 activation
46 alarmins
47 albicans
48 antifungal response
49 balance
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51 cellular damage
52 commensalism
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54 contrast
55 control
56 damage
57 defense
58 degree
59 delayed induction
60 development
61 dichotomy
62 differences
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65 diversity
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67 epithelium
68 experimental model
69 fungal
70 fungal control
71 fungal diversity
72 fungal-host interactions
73 fungi
74 host
75 host immune status
76 host response
77 immune activation
78 immune status
79 immunity
80 induction
81 induction of inflammation
82 infected tissues
83 infection
84 inflammation
85 interaction
86 interleukin
87 intraspecies differences
88 intraspecies diversity
89 isolates
90 kinetics
91 model
92 mucosa
93 mucosal defense
94 neutrophil response
95 neutrophils
96 opportunistic infections
97 oral infection
98 oral mucosa
99 outcomes
100 pathogenicity
101 release
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