Evidence map›Paper›PMID 32634452›Full record

ArticleThe Journal of allergy and clinical immunology2021

Staphylococcus epidermidis protease EcpA can be a deleterious component of the skin microbiome in atopic dermatitis.

Laura Cau, Michael R Williams, Anna M Butcher, Teruaki Nakatsuji, Jeffrey S Kavanaugh, Joyce Y Cheng, Faiza Shafiq, Kyle Higbee, Tissa R Hata, Alexander R Horswill and 1 more

Abstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing 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

112 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. SkinApplied and environmental microbiology · 2026
    Article
  6. Article
  7. Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  8. Dysbiosis in the Pathogenesis of Atopic Dermatitis.The Journal of dermatology · 2026
    Review
  9. Atopic Dermatitis-like mouse model using early inoculation of patient-derivedJID innovations : skin science from molecules to population health · 2026
    Article
  10. Review
  11. The Evolution of Symbiosis inBiomolecules · 2026
    Review
  12. Review
  13. Frontiers in immunology · 2026
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

52 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

11 authors.

Laura CauDepartment of Dermatology, University of California San Diego, San Diego, Calif; R&D Department, SILAB, Brive, France.
Michael R WilliamsDepartment of Dermatology, University of California San Diego, San Diego, Calif.
Anna M ButcherDepartment of Dermatology, University of California San Diego, San Diego, Calif.
Teruaki NakatsujiDepartment of Dermatology, University of California San Diego, San Diego, Calif.
Jeffrey S KavanaughDepartment of Immunology and Microbiology, University of Colorado Anschutz, Medical Campus, Aurora, Colo.
Joyce Y ChengDepartment of Dermatology, University of California San Diego, San Diego, Calif.
Faiza ShafiqDepartment of Dermatology, University of California San Diego, San Diego, Calif.
Kyle HigbeeDepartment of Dermatology, University of California San Diego, San Diego, Calif.
Tissa R HataDepartment of Dermatology, University of California San Diego, San Diego, Calif.
Alexander R HorswillDepartment of Immunology and Microbiology, University of Colorado Anschutz, Medical Campus, Aurora, Colo; Department of Veterans Affairs Eastern Colorado Health Care System, Aurora, Colo.
Richard L GalloDepartment of Dermatology, University of California San Diego, San Diego, Calif; Center for Microbiome Innovation, University of California San Diego, San Diego, Calif. Electronic address: rgallo@ucsd.edu.

Funding

Targeted Microbiome Transplant in Atopic DermatitisU19AI117673 · NIAID · NATIONAL JEWISH HEALTH · PI GALLO, RICHARD L · 2015 to 2019
$30.6M
Cathelicidin in Skin ImmunityR37AI052453 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard L Gallo, Victor Nizet · 2019 to 2026
$4.6M
Quorum sensing, diversity and skin inflammationR01AI153185 · NIAID · UNIVERSITY OF COLORADO DENVER · PI GALLO, RICHARD L, HORSWILL, ALEXANDER R · 2020 to 2024
$3.2M
Conflict and Cooperation between AMP Species on the skinR01AR076082 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GALLO, RICHARD L, NAKATSUJI, TERUAKI · 2019 to 2023
$2.3M
Quorum Sensing Dependent Interactions with Biofilms and Innate Immunity DefensesI01BX002711 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI ALEXANDER R HORSWILL · 2015 to 2026
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BLRD VA I01 BX002711NIAID NIH HHS R01 AI153185NIAID NIH HHS R37 AI052453NIAID NIH HHS U19 AI117673NIAMS NIH HHS R01 AR076082
6 · The paper itself

Abstract

backgroundStaphylococcus aureus and Staphylococcus epidermidis are the most abundant bacteria found on the skin of patients with atopic dermatitis (AD). S aureus is known to exacerbate AD, whereas S epidermidis has been considered a beneficial commensal organism.

objectiveIn this study, we hypothesized that S epidermidis could promote skin damage in AD by the production of a protease that damages the epidermal barrier.

methodsThe protease activity of S epidermidis isolates was compared with that of other staphylococcal species. The capacity of S epidermidis to degrade the barrier and induce inflammation was examined by using human keratinocyte tissue culture and mouse models. Skin swabs from atopic and healthy adult subjects were analyzed for the presence of S epidermidis genomic DNA and mRNA.

resultsS epidermidis strains were observed to produce strong cysteine protease activity when grown at high density. The enzyme responsible for this activity was identified as EcpA, a cysteine protease under quorum sensing control. EcpA was shown to degrade desmoglein-1 and LL-37 in vitro, disrupt the physical barrier, and induce skin inflammation in mice. The abundance of S epidermidis and expression of ecpA mRNA were increased on the skin of some patients with AD, and this correlated with disease severity. Another commensal skin bacterial species, Staphylococcus hominis, can inhibit EcpA production by S epidermidis.

conclusionS epidermidis has commonly been regarded as a beneficial skin microbe, whereas S aureus has been considered deleterious. This study suggests that the overabundance of S epidermidis found on some atopic patients can act similarly to S aureus and damage the skin by expression of a cysteine protease.

Indexed as

MicrobiotaAnimalsAntimicrobial Cationic PeptidesBacterial ProteinsCathelicidinsCells, CulturedCysteine ProteasesDermatitis, AtopicDesmoglein 1DNA, BacterialHumansKeratinocytesMiceMice, Inbred C57BLSeverity of Illness IndexSkinAntimicrobial Cationic PeptidesBacterial ProteinsCathelicidinsCysteine ProteasesDesmoglein 1DNA, BacterialEcpA protein, Staphylococcus epidermidisAtopic dermatitiscytokinedysbiosisepidermal barrierinflammationmicrobiomeproteaseskinStaphylococcus epidermidis

Identifiers

PMID32634452
PMCPMC8058862

What OpenQuestion holds

Textmetadata
LicenceTDM
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.