Evidence map›Paper›PMID 31350436›Full record

ArticleScientific reports2019

The Henna pigment Lawsone activates the Aryl Hydrocarbon Receptor and impacts skin homeostasis.

Laura Lozza, Pedro Moura-Alves, Teresa Domaszewska, Carolina Lage Crespo, Ioana Streata, Annika Kreuchwig, Andreas Puyskens, Marina Bechtle, Marion Klemm, Ulrike Zedler and 15 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 7 institutions in 6 countries.

Laura LozzaDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany. lozza@mpiib-berlin.mpg.de.
Pedro Moura-AlvesDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany. pedro.mouraalves@ludwig.ox.ac.uk.ORCID http://orcid.org/0000-0003-4337-9113
Teresa DomaszewskaDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
Carolina Lage CrespoCEDOC, NOVA Medical School, NOVA University of Lisbon, Lisbon, 1169-056, Portugal.
Ioana StreataHuman Genomics Laboratory - University of Medicine and Pharmacy of Craiova, Craiova, Romania.
Annika KreuchwigLeibniz-Forschungsinstitut fuer Molekulare Pharmakologie (FMP), Robert-Rössle-Strasse 10, 13125, Berlin, Germany.
Andreas PuyskensDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
Marina BechtleDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
Marion KlemmDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
Ulrike ZedlerDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
Bogdan Silviu UngureanuResearch Center of Gastroenterology and Hepatology, University of Medicine and Pharmacy of Craiova, Craiova, Romania.
Ute Guhlich-BornhofDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
Anne-Britta KoehlerDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
Manuela StäberDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
Hans-Joachim MollenkopfMicroarray Core Facility, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.ORCID http://orcid.org/0000-0003-1167-4783
Robert HurwitzBiochemistry and Protein Purification Core Facility, Max Planck Institute for Infection Biology. Charitéplatz 1, D-10117, Berlin, Germany.
Jens FurkertLeibniz-Forschungsinstitut fuer Molekulare Pharmakologie (FMP), Robert-Rössle-Strasse 10, 13125, Berlin, Germany.
Gerd KrauseLeibniz-Forschungsinstitut fuer Molekulare Pharmakologie (FMP), Robert-Rössle-Strasse 10, 13125, Berlin, Germany.
January WeinerDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany.
António JacintoCEDOC, NOVA Medical School, NOVA University of Lisbon, Lisbon, 1169-056, Portugal.
Ioana MihaiHuman Genomics Laboratory - University of Medicine and Pharmacy of Craiova, Craiova, Romania.
Maria Leite-de-MoraesLaboratory of Immunoregulation and Immunopathology, INEM (Institut Necker-Enfants Malades), CNRS UMR8253, INSERM UMR1151 and Paris Descartes University, Paris, France.ORCID http://orcid.org/0000-0002-2891-2269
Frank SiebenhaarDepartment of Dermatology and Allergy, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Marcus MaurerDepartment of Dermatology and Allergy, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Stefan H E KaufmannDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117, Berlin, Germany. kaufmann@mpiib-berlin.mpg.de.ORCID http://orcid.org/0000-0001-9866-8268
Max Planck Institute for Infection Biology · DELeibniz-Forschungsinstitut für Molekulare Pharmakologie · DEUniversity of Medicine and Pharmacy of Craiova · ROCharité - Universitätsmedizin Berlin · DEUniversity of Lisbon · PTCentre National de la Recherche Scientifique · FRInstitute for Advanced Study · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a first host barrier, the skin is constantly exposed to environmental insults that perturb its integrity. Tight regulation of skin homeostasis is largely controlled by the aryl hydrocarbon receptor (AhR). Here, we demonstrate that Henna and its major pigment, the naphthoquinone Lawsone activate AhR, both in vitro and in vivo. In human keratinocytes and epidermis equivalents, Lawsone exposure enhances the production of late epidermal proteins, impacts keratinocyte differentiation and proliferation, and regulates skin inflammation. To determine the potential use of Lawsone for therapeutic application, we harnessed human, murine and zebrafish models. In skin regeneration models, Lawsone interferes with physiological tissue regeneration and inhibits wound healing. Conversely, in a human acute dermatitis model, topical application of a Lawsone-containing cream ameliorates skin irritation. Altogether, our study reveals how a widely used natural plant pigment is sensed by the host receptor AhR, and how the physiopathological context determines beneficial and detrimental outcomes.

Indexed as

AnimalsCells, CulturedDermatitisGuided Tissue RegenerationHomeostasisHumansKeratinocytesLawsonia PlantMiceModels, AnimalNaphthoquinonesReceptors, Aryl HydrocarbonSkinWound HealingZebrafishlawsoneNaphthoquinonesReceptors, Aryl Hydrocarbon

Identifiers

PMID31350436
PMCPMC6659674
OpenAlexW2966778022

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.