Evidence map›Paper›PMID 32214018›Full record

ArticleJournal of clinical medicine2020

Aryl Hydrocarbon Receptor Activation Downregulates IL-33 Expression in Keratinocytes via Ovo-Like 1.

Gaku Tsuji, Akiko Hashimoto-Hachiya, Vu Hai Yen, Sho Miake, Masaki Takemura, Yasutaka Mitamura, Takamichi Ito, Maho Murata, Masutaka Furue, Takeshi Nakahara

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

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  8. Journal of clinical medicine · 2022
    Review
  9. Article
  10. Natural Compounds Tapinarof andFrontiers in immunology · 2022
    Article
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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

10 authors at 2 institutions in 1 country.

Gaku TsujiDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Akiko Hashimoto-HachiyaResearch and Clinical Center for Yusho and Dioxin, Kyushu University Hospital, Fukuoka 812-8582, Japan.
Vu Hai YenDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Sho MiakeDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Masaki TakemuraDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.ORCID 0000-0002-2503-8449
Yasutaka MitamuraDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Takamichi ItoDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Maho MurataDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.ORCID 0000-0002-1068-6873
Masutaka FurueDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.ORCID 0000-0002-2967-1073
Takeshi NakaharaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.ORCID 0000-0003-2811-8273
Kyushu University · JPKyushu University Hospital · JP

Funding

JSPS KAKENHI 17K10213
6 · The paper itself

Abstract

backgroundIL-33, one of the IL-1 superfamily cytokines, has been shown to be associated with pruritus and inflammation in atopic dermatitis (AD). Furthermore, IL-33 production derived from keratinocytes reportedly has a crucial role in the development of AD; however, the mechanism of IL-33 expression has not been fully understood.

methodsWe analyzed IL-33 expression in normal human epidermal keratinocytes (NHEKs) treated with IL-4.

resultsIL-4 induced the upregulation of IL-33 expression in NHEKs. Based on the findings 1) that ovo-like 1 (OVOL1), a susceptible gene of AD, upregulates filaggrin (FLG) and loricrin (LOR) expression in NHEKs and 2) that reduced expression of FLG and LOR leads to production of IL-1 superfamily cytokines, we examined the involvement of OVOL1 in IL-33 expression in NHEKs. Knockdown of OVOL1 induced upregulation of IL-33 expression. Moreover, because Glyteer, an activator of aryl hydrocarbon receptor (AHR), reportedly upregulates OVOL1 expression, we examined whether treatment with Glyteer inhibited IL-33 expression in NHEKs. Treatment with Glyteer inhibited IL-4-induced upregulation of IL-33 expression, which was canceled by knockdown of either AHR or OVOL1.

conclusionsActivation of the AHR-OVOL1 axis inhibits IL-4-induced IL-33 expression, which could be beneficial for the treatment of AD.

Indexed as

aryl hydrocarbon receptoratopic dermatitisIL-33

Identifiers

PMID32214018
PMCPMC7141508
OpenAlexW3013539696

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Registered trials

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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.