Evidence map›Paper›PMID 11292712›Full record

ArticleInfection and immunity2001

Pathogenic yeasts Cryptococcus neoformans and Candida albicans produce immunomodulatory prostaglandins.

M C Noverr, S M Phare, G B Toews, M J Coffey, G B Huffnagle

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03115073 (A Phase IIa Randomized, Active-controlled, Double-blind, Dose-escalation Study in Patients With Vulvovaginal Candidiasis to Evaluate Dose Response Relationship of Clinical Efficacy, Safety and Tolerability of Topically Administered ProF-001), which is not on this map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
6.4field-weighted citation impact, top 3% 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.

NCT03115073 phase2 / phase3completednot on this mapstarted 2017, after this paper: background citation

A Phase IIa Randomized, Active-controlled, Double-blind, Dose-escalation Study in Patients With Vulvovaginal Candidiasis to Evaluate Dose Response Relationship of Clinical Efficacy, Safety and Tolerability of Topically Administered ProF-001

TypeinterventionalSponsorProFem GmbHRan2017 to 2018Enrolled84ConditionsVulvovaginal Candidiasis (VVC)ArmsCandiplus, Clotrimazole
3 · Its place in the literature

Who cites it

125 citing papers in PubMed, 248 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The role ofMicrobiology spectrum · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Discovering a new paradigm: Gut microbiota as a central modulator of sexual health.World journal of gastrointestinal pathophysiology · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Host immune response against fungal biofilms.Current opinion in microbiology · 2024
    Review
  15. Macrophage fate: to kill or not to kill?Infection and immunity · 2024
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review

65 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

5 authors at 1 institution in 1 country.

M C NoverrDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109-0642, USA.
S M Phare
G B Toews
M J Coffey
G B Huffnagle
Pulmonary and Critical Care Associates · US

Funding

Molecular Mechanisms of Microbial Pathogenesis Training ProgramT32AI007528 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARRUTHERS, VERNON BRUCE · 1998 to 2024
$6.8M
NIAID NIH HHS T32 AI007528NIAID NIH HHS T32AI07528Wellcome Trust
6 · The paper itself

Abstract

Enhanced prostaglandin production during fungal infection could be an important factor in promoting fungal colonization and chronic infection. Host cells are one source of prostaglandins; however, another potential source of prostaglandins is the fungal pathogen itself. Our objective was to determine if the pathogenic yeasts Cryptococcus neoformans and Candida albicans produce prostaglandins and, if so, to begin to define the role of these bioactive lipids in yeast biology and disease pathogenesis. C. neoformans and C. albicans both secreted prostaglandins de novo or via conversion of exogenous arachidonic acid. Treatment with cyclooxygenase inhibitors dramatically reduced the viability of the yeast and the production of prostaglandins, suggesting that an essential cyclooxygenase like enzyme may be responsible for fungal prostaglandin production. A PGE series lipid was purified from both C. albicans and C. neoformans and was biologically active on both fungal and mammalian cells. Fungal PGE(x) and synthetic PGE(2) enhanced the yeast-to-hypha transition in C. albicans. Furthermore, in mammalian cells, fungal PGE(x) down-modulated chemokine production, tumor necrosis factor alpha production, and splenocyte proliferation while up-regulating interleukin 10 production. These are all activities previously documented for mammalian PGE(2). Thus, eicosanoids are produced by pathogenic fungi, are critical for growth of the fungi, and can modulate host immune functions. The discovery that pathogenic fungi produce and respond to immunomodulatory eicosanoids reveals a virulence mechanism that has potentially great implications for understanding the mechanisms of chronic fungal infection, immune deviation, and fungi as disease cofactors.

Indexed as

AnimalsCandida albicansCryptococcus neoformansEnzyme-Linked Immunosorbent AssayIndomethacinLymphocyte ActivationMiceMice, Inbred CBAProstaglandinsTumor Necrosis Factor-alphaVirulenceIndomethacinProstaglandinsTumor Necrosis Factor-alpha

Identifiers

PMID11292712
PMCPMC98248
OpenAlexW2097884283

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.