Evidence map›Paper›PMID 39399487›Full record

ArticleFrontiers in immunology2024

Pregnane X receptor reduces particulate matter-induced type 17 inflammation in atopic dermatitis.

Ji Su Lee, Youngae Lee, Sunhyae Jang, Jang-Hee Oh, Dong Hun Lee, Soyun Cho

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

6 authors.

Ji Su Lee *Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Youngae Lee *Department of Dermatology, Seoul National University Hospital, Seoul, Republic of Korea.
Sunhyae JangDepartment of Dermatology, Seoul National University Hospital, Seoul, Republic of Korea.
Jang-Hee OhDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Dong Hun Lee *Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Soyun Cho *Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Epidemiological evidence suggests that particulate matter (PM) exposure can trigger or worsen atopic dermatitis (AD); however, the underlying mechanisms remain unclear. Recently, pregnane X receptor (PXR), a xenobiotic receptor, was reported to be related to skin inflammation in AD. Objectives: This study aimed to explore the effects of PM on AD and investigate the role of PXR in PM-exposed AD. Methods: Results: Topical application of PM significantly increased dermatitis score and skin thickness in AD-like mice. PM treatment increased the mRNA and protein levels of type 17 inflammatory mediators, including interleukin (IL)-17A, IL-23A, IL-1β, and IL-6, in AD-like mice and human keratinocytes. PM also activated PXR signaling, and PXR knockdown exacerbated PM-induced type 17 inflammation in human keratinocytes and mouse CD4 Conclusion: In summary, PM exposure induces type 17 inflammation and PXR activation in AD. PXR activation reduces PM-induced type 17 inflammation by suppressing the NF-κB signaling pathway. Thus, PXR represents a promising therapeutic target for controlling the PM-induced AD aggravation.

Indexed as

Dermatitis, AtopicKeratinocytesParticulate MatterPregnane X ReceptorAnimalsCD4-Positive T-LymphocytesCytokinesDisease Models, AnimalFemaleHaCaT CellsHumansInflammationMaleMiceMice, Inbred BALB CNF-kappa BCytokinesNF-kappa BParticulate MatterPregnane X Receptorair pollutionatopic dermatitisparticulate matterpregnane X receptortype 17 inflammation

Identifiers

PMID39399487
PMCPMC11467722

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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.