Evidence map›Paper›PMID 28552668›Full record

ArticleCell host & microbe2017

β1-Integrin Accumulates in Cystic Fibrosis Luminal Airway Epithelial Membranes and Decreases Sphingosine, Promoting Bacterial Infections.

Heike Grassmé, Brian Henry, Regan Ziobro, Katrin Anne Becker, Joachim Riethmüller, Aaron Gardner, Aaron P Seitz, Joerg Steinmann, Stephan Lang, Christopher Ward and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Cell host & microbe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 101 citations in OpenAlex.

  1. HDAC6 inhibition reducesInfection and immunity · 2026
    Article
  2. Article
  3. Sphingosine synergizes with polymyxin antibiotics againstMicrobiology (Reading, England) · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Ion channels and actin: A tale of two friends.Histology and histopathology · 2025
    Review
  8. Sphingosine kills Mycobacteria and suppresses mycobacterial lung infections.Journal of molecular medicine (Berlin, Germany) · 2025
    Article
  9. Sphingosine-mediated death ofInfection and immunity · 2025
    Article
  10. TheMicrobiology (Reading, England) · 2025
    Article
  11. ThebioRxiv : the preprint server for biology · 2024
    Article
  12. Article
  13. Review
  14. Sphingosine Prevents Rhinoviral Infections.International journal of molecular sciences · 2024
    Article
  15. Article
  16. Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024
    Review
  17. Review
  18. Article
  19. Reduced Sphingosine in Cystic Fibrosis Increases Susceptibility toInternational journal of molecular sciences · 2023
    Article
  20. Review

10 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

16 authors at 7 institutions in 3 countries.

Heike GrassméDepartment of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany.
Brian HenryDepartment of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany; Department of Surgery, University of Cincinnati, 231 Albert Sabin Way, ML 0558, Cincinnati, Ohio 45229, USA.
Regan ZiobroDepartment of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany.
Katrin Anne BeckerDepartment of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany.
Joachim RiethmüllerCenter for Pediatric Clinical Studies, Children's Clinic, University of Tuebingen, Hoppe-Seyler-Strasse 1, 72076 Tübingen, Germany.
Aaron GardnerInstitute of Cellular Medicine, Newcastle University, c/o Level 3, Clinical Resource Building, Great North Children's Hospital, Queen Victoria Road, Newcastle upon Tyne, NE1 4LP, UK.
Aaron P SeitzDepartment of Surgery, University of Cincinnati, 231 Albert Sabin Way, ML 0558, Cincinnati, Ohio 45229, USA.
Joerg SteinmannDepartment of Medical Microbiology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany.
Stephan LangDepartment of Otorhinolaryngology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany.
Christopher WardInstitute of Cellular Medicine, Newcastle University, c/o Level 3, Clinical Resource Building, Great North Children's Hospital, Queen Victoria Road, Newcastle upon Tyne, NE1 4LP, UK.
Edward H SchuchmanDepartment of Genetics & Genomic Sciences, Icahn School of Medicine at Mount Sinai, 1425 Madison Avenue, New York, NY 10029, USA.
Charles C CaldwellDepartment of Surgery, University of Cincinnati, 231 Albert Sabin Way, ML 0558, Cincinnati, Ohio 45229, USA.
Markus KamlerWest German Heart and Vascular Center Essen, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany.
Michael J EdwardsDepartment of Surgery, University of Cincinnati, 231 Albert Sabin Way, ML 0558, Cincinnati, Ohio 45229, USA.
Malcolm BrodlieInstitute of Cellular Medicine, Newcastle University, c/o Level 3, Clinical Resource Building, Great North Children's Hospital, Queen Victoria Road, Newcastle upon Tyne, NE1 4LP, UK.
Erich GulbinsDepartment of Molecular Biology, University of Duisburg-Essen, Hufelandstrasse 55, 45122 Essen, Germany; Department of Surgery, University of Cincinnati, 231 Albert Sabin Way, ML 0558, Cincinnati, Ohio 45229, USA. Electronic address: erich.gulbins@uni-due.de.
University of Duisburg-Essen · DEUniversity of Cincinnati · USNewcastle University · GBSabin Vaccine Institute · USGreat North Children's Hospital · GBIcahn School of Medicine at Mount Sinai · USUniversity Children's Hospital Tübingen · DE

Funding

Short Term Medical Student Training GrantT35DK060444 · NIDDK · UNIVERSITY OF CINCINNATI · PI JASON T BLACKARD · 2002 to 2026
$2.3M
Medical Research Council G0800419Medical Research Council MR/M008797/1NIDDK NIH HHS T35 DK060444
6 · The paper itself

Abstract

Chronic pulmonary colonization with bacterial pathogens, particularly Pseudomonas aeruginosa, is the primary cause of morbidity and mortality in patients with cystic fibrosis (CF). We observed that β1-integrins accumulate on the luminal membrane of upper-airway epithelial cells from mice and humans with CF. β1-integrin accumulation is due to increased ceramide and the formation of ceramide platforms that trap β1-integrins on the luminal pole of bronchial epithelial cells. β1-integrins downregulate acid ceramidase expression, resulting in further accumulation of ceramide and consequent reduction of surface sphingosine, a lipid that kills bacteria. Interrupting this vicious cycle by triggering surface β1-integrin internalization via anti-β1-integrin antibodies or the RGD peptide ligand-or by genetic or pharmacological correction of ceramide levels-normalizes β1-integrin distribution and sphingosine levels in CF epithelial cells and prevents P. aeruginosa infection in CF mice. These findings suggest a therapeutic avenue to ameliorate CF-associated bacterial infections.

Indexed as

Acid CeramidaseAnimalsBacterial InfectionsCell MembraneCeramidesCystic FibrosisEpithelial CellsFemaleHumansIntegrin beta1LungMaleMicePseudomonas aeruginosaPseudomonas InfectionsSphingosineAcid CeramidaseASAH1 protein, humanCeramidesIntegrin beta1Sphingosineacid ceramidaseceramideCystic fibrosisepithelial cellsintegrinmembrane domainspneumoniaPseudomonas aeruginosareceptor clusteringsphingosine

Identifiers

PMID28552668
PMCPMC5475347
OpenAlexW2620186816

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.