Evidence map›Paper›PMID 29069103›Full record

ArticlePLoS pathogens2017

The yeast form of the fungus Candida albicans promotes persistence in the gut of gnotobiotic mice.

Lena Böhm, Sanda Torsin, Su Hlaing Tint, Marie Therese Eckstein, Tobias Ludwig, J Christian Pérez

Abstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
–field-weighted citation impact
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

57 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Commensal colonization ofMicrobiology spectrum · 2025
    Article
  7. Review
  8. Article
  9. Review
  10. Microbiology and molecular biology reviews : MMBR · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Commensal fungi in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2023
    Review
  16. Article
  17. Aneuploidy and gene dosage regulate filamentation and host colonization byProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Article
  19. iScience · 2023
    Review
  20. Review
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

6 authors.

Lena BöhmInterdisciplinary Center for Clinical Research, University Hospital Würzburg, Würzburg, Germany.ORCID http://orcid.org/0000-0002-5520-0427
Sanda TorsinInterdisciplinary Center for Clinical Research, University Hospital Würzburg, Würzburg, Germany.
Su Hlaing TintInterdisciplinary Center for Clinical Research, University Hospital Würzburg, Würzburg, Germany.
Marie Therese EcksteinInterdisciplinary Center for Clinical Research, University Hospital Würzburg, Würzburg, Germany.
Tobias LudwigInterdisciplinary Center for Clinical Research, University Hospital Würzburg, Würzburg, Germany.ORCID http://orcid.org/0000-0003-2436-7707
J Christian PérezInterdisciplinary Center for Clinical Research, University Hospital Würzburg, Würzburg, Germany.ORCID http://orcid.org/0000-0001-5790-1481

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many microorganisms that cause systemic, life-threatening infections in humans reside as harmless commensals in our digestive tract. Yet little is known about the biology of these microbes in the gut. Here, we visualize the interface between the human commensal and pathogenic fungus Candida albicans and the intestine of mice, a surrogate host. Because the indigenous mouse microbiota restricts C. albicans settlement, we compared the patterns of colonization in the gut of germ free and antibiotic-treated conventionally raised mice. In contrast to the heterogeneous morphologies found in the latter, we establish that in germ free animals the fungus almost uniformly adopts the yeast cell form, a proxy of its commensal state. By screening a collection of C. albicans transcription regulator deletion mutants in gnotobiotic mice, we identify several genes previously unknown to contribute to in vivo fitness. We investigate three of these regulators-ZCF8, ZFU2 and TRY4-and show that indeed they favor the yeast form over other morphologies. Consistent with this finding, we demonstrate that genetically inducing non-yeast cell morphologies is detrimental to the fitness of C. albicans in the gut. Furthermore, the identified regulators promote adherence of the fungus to a surface covered with mucin and to mucus-producing intestinal epithelial cells. In agreement with this result, histology sections indicate that C. albicans dwells in the murine gut in close proximity to the mucus layer. Thus, our findings reveal a set of regulators that endows C. albicans with the ability to endure in the intestine through multiple mechanisms.

Indexed as

AnimalsCandida albicansCandidiasisGerm-Free LifeHost-Pathogen InteractionsIntestinal MucosaLife Cycle StagesMiceSymbiosis

Identifiers

PMID29069103
PMCPMC5673237

What OpenQuestion holds

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LicenceCC BY
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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.