Evidence map›Paper›PMID 34986357›Full record

ArticleCell reports2022

Estrogen promotes innate immune evasion of Candida albicans through inactivation of the alternative complement system.

Pizga Kumwenda, Fabien Cottier, Alexandra C Hendry, Davey Kneafsey, Ben Keevan, Hannah Gallagher, Hung-Ji Tsai, Rebecca A Hall

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
6.8field-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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  5. Article
  6. Review
  7. Article
  8. Species Distribution and Determinants ofMedicina (Kaunas, Lithuania) · 2026
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  18. Vaginal Clinical Isolates ofJournal of fungi (Basel, Switzerland) · 2025
    Article
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  20. Article
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

8 authors at 2 institutions in 1 country.

Pizga KumwendaInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK.
Fabien CottierInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK.
Alexandra C HendryKent Fungal Group, Division of Natural Sciences, School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.
Davey KneafseyKent Fungal Group, Division of Natural Sciences, School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.
Ben KeevanInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK.
Hannah GallagherInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK.
Hung-Ji TsaiInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK.
Rebecca A HallInstitute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK; Kent Fungal Group, Division of Natural Sciences, School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK. Electronic address: r.a.hall@kent.ac.uk.
University of Birmingham · GBUniversity of Kent · GB

Funding

Biotechnology and Biological Sciences Research Council BB/R00966X/1Biotechnology and Biological Sciences Research Council BB/R00966X/2Medical Research Council MR/L00903X/1Wellcome TrustWellcome Trust 097377/Z/11/Z
6 · The paper itself

Abstract

Candida albicans is a commensal of the urogenital tract and the predominant cause of vulvovaginal candidiasis (VVC). Factors that increase circulatory estrogen levels such as pregnancy, the use of oral contraceptives, and hormone replacement therapy predispose women to VVC, but the reasons for this are largely unknown. Here, we investigate how adaptation of C. albicans to estrogen impacts the fungal host-pathogen interaction. Estrogen promotes fungal virulence by enabling C. albicans to avoid the actions of the innate immune system. Estrogen-induced innate immune evasion is mediated via inhibition of opsonophagocytosis through enhanced acquisition of the human complement regulatory protein, Factor H, on the fungal cell surface. Estrogen-induced accumulation of Factor H is dependent on the fungal cell surface protein Gpd2. The discovery of this hormone-sensing pathway might pave the way in explaining gender biases associated with fungal infections and may provide an alternative approach to improving women's health.

Indexed as

Candida albicansCandidiasis, VulvovaginalComplement Factor HComplement Pathway, AlternativeEstrogensFemaleGlycerol-3-Phosphate Dehydrogenase (NAD+)HumansImmune EvasionImmunity, InnatePhagocytosisProgesteroneVirulenceComplement Factor HEstrogensGlycerol-3-Phosphate Dehydrogenase (NAD+)ProgesteroneCandida albicanscomplementFactor HGpd2hormone sensingInnate immune evasionoestrogenVVC

Identifiers

PMID34986357
PMCPMC8755443
OpenAlexW4205649825

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.