Evidence map›Paper›PMID 26320997›Full record

ArticleCell host & microbe2015

Staphylococcus aureus Targets the Duffy Antigen Receptor for Chemokines (DARC) to Lyse Erythrocytes.

András N Spaan, Tamara Reyes-Robles, Cédric Badiou, Sylvie Cochet, Kristina M Boguslawski, Pauline Yoong, Christopher J Day, Carla J C de Haas, Kok P M van Kessel, François Vandenesch and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

72 citing papers in PubMed, 111 citations in OpenAlex.

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  10. Linking Virulence and Iron Limitation Response inJournal of proteome research · 2025
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  11. A promisingClinical and experimental vaccine research · 2025
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  15. Atypical chemokine receptors in the immune system.Nature reviews. Immunology · 2024
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 4 countries.

András N SpaanCIRI, Inserm U1111, CNRS UMR 5308, Lyon, France; Université Claude Bernard Lyon-1, Ecole Normale Supérieure, 69007 Lyon, France; Department of Medical Microbiology, University Medical Center Utrecht, 3584CX Utrecht, The Netherlands.
Tamara Reyes-RoblesDepartment of Microbiology, New York University School of Medicine, NY 10016, USA.
Cédric BadiouCIRI, Inserm U1111, CNRS UMR 5308, Lyon, France; Université Claude Bernard Lyon-1, Ecole Normale Supérieure, 69007 Lyon, France.
Sylvie CochetInserm U1134, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, UMR_S1134, Paris, France; Institut National de la Transfusion Sanguine, F-75739 Paris, France; Laboratoire d'Excellence GR-Ex, 75238 Paris, France.
Kristina M BoguslawskiDepartment of Microbiology, New York University School of Medicine, NY 10016, USA.
Pauline YoongDepartment of Microbiology, New York University School of Medicine, NY 10016, USA.
Christopher J DayInstitute for Glycomics, Griffith University, Gold Coast, Queensland 4222, Australia.
Carla J C de HaasDepartment of Medical Microbiology, University Medical Center Utrecht, 3584CX Utrecht, The Netherlands.
Kok P M van KesselDepartment of Medical Microbiology, University Medical Center Utrecht, 3584CX Utrecht, The Netherlands.
François VandeneschCIRI, Inserm U1111, CNRS UMR 5308, Lyon, France; Université Claude Bernard Lyon-1, Ecole Normale Supérieure, 69007 Lyon, France; Hospices Civils de Lyon, 69007 Lyon, France.
Michael P JenningsInstitute for Glycomics, Griffith University, Gold Coast, Queensland 4222, Australia.
Caroline Le Van KimInserm U1134, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, UMR_S1134, Paris, France; Institut National de la Transfusion Sanguine, F-75739 Paris, France; Laboratoire d'Excellence GR-Ex, 75238 Paris, France.
Yves ColinInserm U1134, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, UMR_S1134, Paris, France; Institut National de la Transfusion Sanguine, F-75739 Paris, France; Laboratoire d'Excellence GR-Ex, 75238 Paris, France.
Jos A G van StrijpDepartment of Medical Microbiology, University Medical Center Utrecht, 3584CX Utrecht, The Netherlands.
Thomas HenryCIRI, Inserm U1111, CNRS UMR 5308, Lyon, France; Université Claude Bernard Lyon-1, Ecole Normale Supérieure, 69007 Lyon, France. Electronic address: thomas.henry@inserm.fr.
Victor J TorresDepartment of Microbiology, New York University School of Medicine, NY 10016, USA. Electronic address: victor.torres@nyumc.org.
New York University · USUniversité Claude Bernard Lyon 1 · FRInserm · FRUniversity Medical Center Utrecht · NLGriffith University · AU

Funding

MEDICAL SCIENTIST TRAININGT32GM007308 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PHILIPS, MARK REID · 1985 to 2019
$23.2M
INFECTIOUS DISEASES &BASIC MICROBIOLOGICAL MECHANISMST32AI007180 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WEISER, JEFFREY NEAL · 1985 to 2022
$8.9M
Mechanistic Studies Of The Staphylococcus aureus LukAB CytotoxinR01AI099394 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Victor J. Torres · 2013 to 2026
$6.1M
Contribution of LukED to Staphylococcus aureus pathobiologyR01AI105129 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI TORRES, VICTOR J. · 2014 to 2023
$4.9M
Molecular and Cellular Basis of Toxin Mediated Pathogenesis in Staphylococcus aurF32AI098395 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ALONZO, FRANCIS · 2012 to 2013
$94k
Staphylococcus aureus mediated targeting and killing of immune cellsF31AI112290 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI REYES-ROBLES, TAMARA · 2014 to 2015
$62k
NIAID NIH HHS F31 AI112290NIAID NIH HHS F32 AI098395NIAID NIH HHS R01 AI099394NIAID NIH HHS R01 AI105129NIAID NIH HHS T32 AI007180NIGMS NIH HHS T32 GM007308
6 · The paper itself

Abstract

In order for Staphylococcus aureus to thrive inside the mammalian host, the bacterium has to overcome iron scarcity. S. aureus is thought to produce toxins that lyse erythrocytes, releasing hemoglobin, the most abundant iron source in mammals. Here we identify the Duffy antigen receptor for chemokines (DARC) as the receptor for the S. aureus hemolytic leukocidins LukED and HlgAB. By assessing human erythrocytes with DARC polymorphisms, we determined that HlgAB- and LukED-mediated lysis directly relates to DARC expression. DARC is required for S. aureus-mediated lysis of human erythrocytes, and DARC overexpression is sufficient to render cells susceptible to toxin-mediated lysis. HlgA and LukE bind directly to DARC through different regions, and by targeting DARC, HlgAB and LukED support S. aureus growth in a hemoglobin-acquisition-dependent manner. These findings elucidate how S. aureus targets and lyses erythrocytes to release one of the scarcest nutrients within the mammalian host.

Indexed as

HemolysisHost-Pathogen InteractionsDuffy Blood-Group SystemErythrocytesHumansLeukocidinsProtein BindingReceptors, Cell SurfaceStaphylococcus aureusACKR1 protein, humanDuffy Blood-Group SystemLeukocidinsReceptors, Cell Surface

Identifiers

PMID26320997
PMCPMC4578157
OpenAlexW1941322164

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Registered trials

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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.