Evidence map›Paper›PMID 28176789›Full record

ArticleMucosal immunology2017

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

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 and 4 more

Open access · bronzeAbstract read
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In one paragraph

Article in Mucosal immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
8.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

87 citing papers in PubMed, 126 citations in OpenAlex.

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  6. Exometabolome variation in the fungal pathogen of humansApplied and environmental microbiology · 2026
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  20. Neutrophils: emerging perspectives on the pathogenesis of oral mucosal diseases.Frontiers in cellular and infection microbiology · 2025
    Review

27 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 3 countries.

F A SchönherrSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
F SparberSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
F R KirchnerSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
E GuiducciSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
K Trautwein-WeidnerSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
A GladiatorSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
N SertourInstitut Pasteur, INRA, Unité Biologie et Pathogénicité Fongiques, Paris, France.
U HetzelInstitute of Veterinary Pathology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
G T T LeSingapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
N PavelkaSingapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
C d'EnfertInstitut Pasteur, INRA, Unité Biologie et Pathogénicité Fongiques, Paris, France.
M-E BougnouxInstitut Pasteur, INRA, Unité Biologie et Pathogénicité Fongiques, Paris, France.
C F CortiLaboratory of Applied Microbiology, DACD, SUPSI, Bellinzona, Switzerland.
S LeibundGut-LandmannSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
University of Zurich · CHAgency for Science, Technology and Research · SGInstitut Pasteur · FRUniversity of Applied Sciences and Arts of Southern Switzerland · CHHôpital Necker-Enfants Malades · FR

Funding

Swiss National Science Foundation 150758
6 · The paper itself

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.

Indexed as

AlarminsBacterial ProteinsBiodiversityCandida albicansCandidiasisCell LineCell MovementHost-Pathogen InteractionsHumansImmunity, MucosalInterleukin-17KeratinocytesMouth MucosaNeutrophilsSignal TransductionSpecies SpecificityAlarminsBacterial ProteinsInterleukin-17

Identifiers

PMID28176789
OpenAlexW2587625629

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.