Evidence map›Paper›PMID 27702565›Full record

ArticleThe Journal of investigative dermatology2017

IL-1β-Induced Protection of Keratinocytes against Staphylococcus aureus-Secreted Proteases Is Mediated by Human β-Defensin 2.

Bingjie Wang, Brian J McHugh, Ayub Qureshi, Dominic J Campopiano, David J Clarke, J Ross Fitzgerald, Julia R Dorin, Richard Weller, Donald J Davidson

Open access · hybridAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. An Ex Vivo 'Microorganisms · 2026
    Article
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  5. Interaction BetweenCurrent pharmaceutical biotechnology · 2026
    Review
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  9. Article
  10. Article
  11. Article
  12. Human beta defensin-2 protects the epithelial barrier during methicillin-resistantFrontiers in cellular and infection microbiology · 2025
    Article
  13. Review
  14. DNA and cell biology · 2024
    Review
  15. Article
  16. Article
  17. Protocatechuic Acid and Syringin fromCurrent issues in molecular biology · 2023
    Article
  18. Article
  19. Article
  20. Article
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

9 authors at 1 institution in 1 country.

Bingjie WangMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK.
Brian J McHughMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK.
Ayub QureshiMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK.
Dominic J CampopianoSchool of Chemistry, University of Edinburgh, Edinburgh, UK.
David J ClarkeSchool of Chemistry, University of Edinburgh, Edinburgh, UK.
J Ross FitzgeraldThe Roslin Institute and Edinburgh Infectious Diseases, University of Edinburgh, Easter Bush, Midlothian, UK.
Julia R DorinMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK.
Richard WellerMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK.
Donald J DavidsonMRC Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, UK. Electronic address: donald.davidson@ed.ac.uk.
University of Edinburgh · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J004227/1Medical Research Council G0901697Medical Research Council G1002046Medical Research Council MR/P02338X/1
6 · The paper itself

Abstract

Atopic dermatitis (AD) is a common chronic inflammatory skin disease that results in significant morbidity. A hallmark of AD is disruption of the critical barrier function of upper epidermal layers, causatively linked to environmental stimuli, genetics, and infection, and a critical current target for the development of new therapeutic and prophylactic interventions. Staphylococcus aureus is an AD-associated pathogen producing virulence factors that induce skin barrier disruption in vivo and contribute to AD pathogenesis. We show, using immortalized and primary keratinocytes, that S. aureus protease SspA/V8 is the dominant secreted factor (in laboratory and AD clinical strains of S. aureus) inducing barrier integrity impairment and tight junction damage. V8-induced integrity damage was inhibited by an IL-1β-mediated mechanism, independent of effects on claudin-1. Induction of keratinocyte expression of the antimicrobial/host defense peptide human β-defensin 2 (hBD2) was found to be the mechanism underpinning this protective effect. Endogenous hBD2 expression was required and sufficient for protection against V8 protease-mediated integrity damage, and exogenous application of hBD2 was protective. This modulatory property of hBD2, unrelated to antibacterial effects, gives new significance to the defective induction of hBD2 in the barrier-defective skin lesions of AD and indicates therapeutic potential.

Indexed as

Analysis of VarianceApoptosisbeta-DefensinsBlotting, WesternCells, CulturedDermatitis, AtopicEnzyme-Linked Immunosorbent AssayEpidermal CellsEpidermisHumansInterleukin-1betaKeratinocytesPeptide HydrolasesReal-Time Polymerase Chain ReactionStaphylococcal Skin InfectionsStaphylococcus aureusbeta-DefensinsInterleukin-1betaPeptide Hydrolases

Identifiers

PMID27702565
PMCPMC5176011
OpenAlexW2529205539

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.