Evidence map›Paper›PMID 1588285›Full record

ArticleThe Journal of experimental medicine1992

A role for complement receptor-like molecules in iron acquisition by Candida albicans.

M A Moors, T L Stull, K J Blank, H R Buckley, D M Mosser

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Article
  2. Article
  3. Genetic Analysis ofJournal of fungi (Basel, Switzerland) · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Cation Transporters ofBiomolecules · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Mechanisms of PathogenicFrontiers in cellular and infection microbiology · 2020
    Review
  13. Pathogens (Basel, Switzerland) · 2019
    Review
  14. Article
  15. Iron at the Centre ofFrontiers in cellular and infection microbiology · 2018
    Review
  16. Metals in fungal virulence.FEMS microbiology reviews · 2018
    Review
  17. Frontiers in microbiology · 2017
    Article
  18. Review
  19. Article
  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

5 authors.

M A MoorsDepartment of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
T L Stull
K J Blank
H R Buckley
D M Mosser

Funding

MOLECULAR ANALYSIS OF H INFLUENZAE HEMOGLOBIN BINDINGR01AI029611 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI STULL, TERRENCE L · 1991 to 2012
$3.3M
Haemophilus influenzae iron/heme regulonR56AI029611 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI STULL, TERRENCE L · 2007 to 2007
$330k
MURINE RETROVIRUS INFECTION AND RESISTANCE TO CANDIDAR01AI027766 · NIAID · TEMPLE UNIVERSITY · PI BLANK, KENNETH J. · 1989 to 1993
–
CANDIDA DIMORPHISM--VIRULENCE &IMMUNOMODULATORY ACTIONR01AI028372 · NIAID · TEMPLE UNIVERSITY · PI ROGERS, THOMAS J · 1990 to 1992
–
NIAID NIH HHS AI-27766NIAID NIH HHS AI-28372NIAID NIH HHS AI-29611
6 · The paper itself

Abstract

Candida albicans, an opportunistic fungal pathogen of humans, is dependent upon iron for growth. Consequently, human serum inhibits C. albicans growth due to the presence of high affinity iron-binding proteins that sequester serum iron, making it unavailable for use by the organism. We report that in the inhibitory environment of human serum, the growth of C. albicans can be restored by the addition of exogenous hemoglobin or heme, but not by protoporphyrin IX, the heme precursor that does not contain iron. We further report that C. albicans can utilize cell surface proteins that are homologues of the mammalian complement receptors (CR) to rosette complement-coated red blood cells (RBC) and obtain RBC-derived iron for growth. The ability of Candida to acquire RBC-derived iron under these conditions is dependent upon Candida-RBC rosetting mediated by CR-like molecules. Unopsonized RBC do not support Candida growth in serum, and restoration of Candida growth in serum by complement-opsonized RBC is inhibited by monoclonal antibodies to the human CR type 3 (CR3). In addition, activation of the human alternative pathway of complement by Candida leads to "bystander" deposition of C3 fragments on the surface of autologous, unopsonized RBC, generating the ligands necessary for Candida-RBC rosetting. These results suggest that C. albicans has evolved a unique strategy for acquiring iron from the host, which exploits the host complement system, and which may contribute to the pathogenic potential of the organism.

Indexed as

NitratesAnimalsAntibodies, MonoclonalBloodCandida albicansComplement Pathway, AlternativeComplement System ProteinsCulture MediaEdetic AcidErythrocytesFerric CompoundsGlucoseHemoglobinsHumansIronKineticsAntibodies, MonoclonalComplement System ProteinsCulture MediaEdetic AcidFerric Compoundsferric nitrateGlucoseHemoglobinsIronNitratesReceptors, Complement

Identifiers

PMID1588285
PMCPMC2119266

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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.