Evidence map›Paper›PMID 24625558›Full record

ArticlePloS one2014

Candida albicans uses the surface protein Gpm1 to attach to human endothelial cells and to keratinocytes via the adhesive protein vitronectin.

Crisanto M Lopez, Reinhard Wallich, Kristian Riesbeck, Christine Skerka, Peter F Zipfel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 59 citations in OpenAlex.

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  12. Interactions Between PathogenicFrontiers in cellular and infection microbiology · 2021
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  13. Review
  14. Review
  15. Frontiers in immunology · 2020
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  16. Mechanisms of PathogenicFrontiers in cellular and infection microbiology · 2020
    Review
  17. Protein markers forJournal of extracellular vesicles · 2020
    Article
  18. Article
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  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 at 4 institutions in 2 countries.

Crisanto M LopezDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology (Hans Knöll Institute), Jena, Germany.
Reinhard WallichInstitute of Immunology, University of Heidelberg, Heidelberg, Germany.
Kristian RiesbeckMedical Microbiology, Department of Laboratory Medicine Malmö, Lund University, Malmö, Sweden.
Christine SkerkaDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology (Hans Knöll Institute), Jena, Germany.
Peter F ZipfelDepartment of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology (Hans Knöll Institute), Jena, Germany; Friedrich Schiller University, Jena, Germany.
Leibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DEHeidelberg University · DELeibniz Association · DELund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Candida albicans is a major cause of invasive fungal infections worldwide. Upon infection and when in contact with human plasma as well as body fluids the fungus is challenged by the activated complement system a central part of the human innate immune response. C. albicans controls and evades host complement attack by binding several human complement regulators like Factor H, Factor H-like protein 1 and C4BP to the surface. Gpm1 (Phosphoglycerate mutase 1) is one fungal Factor H/FHL1 -binding protein. As Gpm1 is surface exposed, we asked whether Gpm1 also contributes to host cell attachment. Here, we show by flow cytometry and by laser scanning microscopy that candida Gpm1 binds to human umbilical vein endothelial cells (HUVEC) to keratinocytes (HaCaT), and also to monocytic U937 cells. Wild type candida did bind, but the candida gpm1Δ/Δ knock-out mutant did not bind to these human cells. In addition Gpm1 when attached to latex beads also conferred attachment to human endothelial cells. When analyzing Gpm1-binding to a panel of extracellular matrix proteins, the human glycoprotein vitronectin was identified as a new Gpm1 ligand. Vitronectin is a component of the extracellular matrix and also a regulator of the terminal complement pathway. Vitronectin is present on the surface of HUVEC and keratinocytes and acts as a surface ligand for fungal Gpm1. Gpm1 and vitronectin colocalize on the surface of HUVEC and HaCaT as revealed by laser scanning microscopy. The Gpm1 vitronectin interaction is inhibited by heparin and the interaction is also ionic strength dependent. Taken together, Gpm1 the candida surface protein binds to vitronectin and mediates fungal adhesion to human endothelial cells. Thus fungal Gpm1 and human vitronectin represent a new set of proteins that are relevant for fungal attachment to human cells interaction. Blockade of the Gpm1 vitronectin interaction might provide a new target for therapy.

Indexed as

Gene Expression Regulation, FungalBiotinylationCandida albicansComplement System ProteinsEndothelial CellsExtracellular MatrixHumansHuman Umbilical Vein Endothelial CellsImmunity, InnateKeratinocytesMutationPhosphoglycerate MutaseProtein BindingRecombinant ProteinsU937 CellsVirulence FactorsComplement System ProteinsGpm1 protein, Candida albicansPhosphoglycerate MutaseRecombinant ProteinsVirulence FactorsVitronectin

Identifiers

PMID24625558
PMCPMC3953207
OpenAlexW1992685096

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.