Evidence map›Paper›PMID 29288652›Full record

ArticleThe Journal of investigative dermatology2018

Co-Activation of Glucocorticoid Receptor and Peroxisome Proliferator-Activated Receptor-γ in Murine Skin Prevents Worsening of Atopic March.

Julie Deckers, Nadia Bougarne, Viacheslav Mylka, Sofie Desmet, Astrid Luypaert, Michael Devos, Giel Tanghe, Justine Van Moorleghem, Manon Vanheerswynghels, Lode De Cauwer and 6 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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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 2 institutions in 1 country.

Julie DeckersNuclear Receptor Lab, Ghent University, Ghent, Belgium; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium; Laboratory of Immunoregulation, VIB Center for Inflammation Research, Department of Internal Medicine, Ghent University, Ghent, Belgium.
Nadia BougarneNuclear Receptor Lab, Ghent University, Ghent, Belgium; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium.
Viacheslav MylkaNuclear Receptor Lab, Ghent University, Ghent, Belgium; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium.
Sofie DesmetNuclear Receptor Lab, Ghent University, Ghent, Belgium; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium.
Astrid LuypaertNuclear Receptor Lab, Ghent University, Ghent, Belgium; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium.
Michael DevosMolecular Signaling and Cell Death Unit, VIB Center for Inflammation Research, Department for Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Giel TangheMolecular Signaling and Cell Death Unit, VIB Center for Inflammation Research, Department for Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Justine Van MoorleghemLaboratory of Immunoregulation, VIB Center for Inflammation Research, Department of Internal Medicine, Ghent University, Ghent, Belgium.
Manon VanheerswynghelsLaboratory of Immunoregulation, VIB Center for Inflammation Research, Department of Internal Medicine, Ghent University, Ghent, Belgium.
Lode De CauwerNuclear Receptor Lab, Ghent University, Ghent, Belgium; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium.
Jonathan ThommisNuclear Receptor Lab, Ghent University, Ghent, Belgium; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium.
Marnik VuylstekeGNOMIXX bvba, Statistics for Genomics, Ghent, Belgium.
Jan TavernierReceptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium.
Bart N LambrechtLaboratory of Immunoregulation, VIB Center for Inflammation Research, Department of Internal Medicine, Ghent University, Ghent, Belgium.
Hamida HammadLaboratory of Immunoregulation, VIB Center for Inflammation Research, Department of Internal Medicine, Ghent University, Ghent, Belgium.
Karolien De BosscherNuclear Receptor Lab, Ghent University, Ghent, Belgium; Receptor Research Laboratories, VIB Center for Medical Biotechnology, Department of Biochemistry, Ghent University, Ghent, Belgium. Electronic address: karolien.debosscher@vib-ugent.be.
Ghent University Hospital · BEGhent University · BE

Funding

European Research Council 789384
6 · The paper itself

Abstract

Children with atopic dermatitis show an increased risk to develop asthma later in life, a phenomenon referred to as "atopic march," which emphasizes the need for secondary prevention therapies. This study aimed to investigate whether relief of skin inflammation by glucocorticoids and peroxisome proliferator-activated receptor agonists might influence the subsequent development of asthma in a murine model for the atopic march in which mice were repeatedly exposed to house dust mite via the skin, followed by exposure to house dust mite in lungs. To abrogate atopic dermatitis, mice received topical treatment with glucocorticoid receptor/peroxisome proliferator-activated receptor-γ agonists. Nuclear receptor ligand effects were assessed on primary keratinocytes and dendritic cells, as central players in skin inflammation. Prior house dust mite-induced skin inflammation aggravates allergic airway inflammation and induces a mixed T helper type 2/T helper type 17 response in the lungs. Cutaneous combined activation of glucocorticoid receptor/peroxisome proliferator-activated receptor-γ reduced skin inflammation to a higher extent compared to single activation. Additive anti-inflammatory effects were more prominent in dendritic cells, as compared to keratinocytes. Alleviation of allergic skin inflammation by activation of glucocorticoid receptor/peroxisome proliferator-activated receptor-γ appeared insufficient to avoid the allergic immune response in the lungs, but efficiently reduced asthma severity by counteracting the Th17 response. Glucocorticoid receptor/peroxisome proliferator-activated receptor-γ co-activation represents a potent remedy against allergic skin inflammation and worsening of atopic march.

Indexed as

Administration, CutaneousAnimalsAsthmaDendritic CellsDermatitis, AtopicDisease Models, AnimalFemaleGlucocorticoidsHumansKeratinocytesLungMiceMice, Inbred C57BLPPAR gammaPrimary Cell CulturePyroglyphidaeGlucocorticoidsPPAR gammaReceptors, Glucocorticoid

Identifiers

PMID29288652
PMCPMC7611015
OpenAlexW2777479722

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.