Evidence map›Paper›PMID 30093649›Full record

ArticleScientific reports2018

Topical administration of EGF suppresses immune response and protects skin barrier in DNCB-induced atopic dermatitis in NC/Nga mice.

Young-Je Kim, Mi Ji Choi, Dong-Ho Bak, Byung Chul Lee, Eun Jung Ko, Ga Ram Ahn, Seung Won Ahn, Moo Joong Kim, Jungtae Na, Beom Joon Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 91 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

10 authors at 4 institutions in 2 countries.

Young-Je KimDepartment of Dermatology, College of Medicine, Chung-Ang University, Seoul, 06973, Korea.
Mi Ji ChoiDepartment of Dermatology, College of Medicine, Chung-Ang University, Seoul, 06973, Korea.ORCID 0000-0003-0118-887X
Dong-Ho BakDepartment of Dermatology, College of Medicine, Chung-Ang University, Seoul, 06973, Korea.
Byung Chul LeeDepartment of Dermatology, College of Medicine, Chung-Ang University, Seoul, 06973, Korea.
Eun Jung KoMyongji Hospital, College of Medicine, Seonam University, Goyang, 10475, Korea.
Ga Ram AhnDepartment of Dermatology, College of Medicine, Chung-Ang University, Seoul, 06973, Korea.
Seung Won AhnOracle Dermatologic Clinic, Seoul, 06103, Korea.
Moo Joong KimFort Hays State University, Hays, Kansas, 67601, USA.
Jungtae NaDepartment of Dermatology, College of Medicine, Chung-Ang University, Seoul, 06973, Korea. pugokjebi@gmail.com.ORCID 0000-0003-1296-4010
Beom Joon KimDepartment of Dermatology, College of Medicine, Chung-Ang University, Seoul, 06973, Korea. beomjoon74@gmail.com.ORCID 0000-0003-2320-7621
Chung-Ang University · KRFort Hays State University · USOracle (United States) · USSeonam University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a common inflammatory skin disease characterized by a complex, heterogeneous pathogenesis including skin barrier dysfunction, immunology, and pruritus. Although epidermal growth factor (EGF) is essential for epithelial homeostasis and wound healing, the effect of EGF on AD remains to be explored. To develop a new therapy for AD, the anti-AD potential of EGF was investigated by inducing AD-like skin lesions in NC/Nga mice using 2,4-dinitrochlorobenzene (DNCB). EGF was administrated to NC/Nga mice to evaluate its therapeutic effect on DNCB-induced AD. EGF treatment improved dermatitis score, ear thickness, epidermal hyperplasia, serum total immunoglobulin E level, and transepidermal water loss in NC/Nga mice with DNCB-induced AD. In addition, levels of skin barrier-related proteins such as filaggrin, involucrin, loricrin, occludin, and zonula occludens-1 (ZO-1) were increased by EGF treatment. These beneficial effects of EGF on AD may be mediated by EGF regulation of Th1/Th2-mediated cytokines, mast cell hyperplasia, and protease activated receptor-2 (PAR-2) and thymic stromal lymphopoietin (TSLP), which are triggers of AD. Taken together, our findings suggest that EGF may potentially protect against AD lesional skin via regulation of skin barrier function and immune response.

Indexed as

Administration, TopicalAnimalsCytokinesDermatitis, AtopicDinitrochlorobenzeneEpidermal Growth FactorFilaggrin ProteinsIntermediate Filament ProteinsMaleMast CellsMiceProtective AgentsReceptor, PAR-2SkinThymic Stromal LymphopoietinZonula Occludens-1 ProteinCytokinesDinitrochlorobenzeneEpidermal Growth FactorF2rl1 protein, mouseFilaggrin ProteinsIntermediate Filament ProteinsProtective AgentsReceptor, PAR-2Thymic Stromal LymphopoietinTjp1 protein, mouseTSLP protein, mouseZonula Occludens-1 Protein

Identifiers

PMID30093649
PMCPMC6085286
OpenAlexW2885267330

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.