mRNAs in skin surface lipids unveiled atopic dermatitis at 1 month.


Journal

Journal of the European Academy of Dermatology and Venereology : JEADV
ISSN: 1468-3083
Titre abrégé: J Eur Acad Dermatol Venereol
Pays: England
ID NLM: 9216037

Informations de publication

Date de publication:
Jul 2023
Historique:
received: 19 07 2022
accepted: 07 02 2023
medline: 14 6 2023
pubmed: 11 3 2023
entrez: 10 3 2023
Statut: ppublish

Résumé

The molecular pathogenesis of atopic dermatitis (AD), presenting skin barrier dysfunction and abnormal inflammations around 1-2 months, is unreported. We aimed to examine the molecular pathogenesis of very early-onset AD by skin surface lipid-RNA (SSL-RNA) using a non-invasive technology in infants aged 1 and 2 months from a prospective cohort. We collected sebum by oil-blotting film of infants aged 1 and 2 months and analysed RNAs in their sebum. We diagnosed AD according to the United Kingdom Working Party's criteria. Infants with AD aged 1 month showed lower expression of genes related to various lipid metabolism and synthesis, antimicrobial peptides, tight junctions, desmosomes and keratinization. They also had higher expression of several genes involved in Th2-, Th17- and Th22-type immune responses and lower expression of negative regulators of inflammation. In addition, gene expressions related to innate immunity were higher in AD infants. Infants aged 1 month with neonatal acne and diagnosed with AD aged 2 months already had gene expression patterns similar to AD aged 1 month in terms of redox, lipid synthesis, metabolism and barrier-related gene expression. We identified molecular changes in barrier function and inflammatory markers that characterize the pathophysiology of AD in infants aged 1 month. We also revealed that neonatal acne at 1 month could predict the subsequent development of AD by sebum transcriptome data.

Sections du résumé

BACKGROUND BACKGROUND
The molecular pathogenesis of atopic dermatitis (AD), presenting skin barrier dysfunction and abnormal inflammations around 1-2 months, is unreported.
OBJECTIVE OBJECTIVE
We aimed to examine the molecular pathogenesis of very early-onset AD by skin surface lipid-RNA (SSL-RNA) using a non-invasive technology in infants aged 1 and 2 months from a prospective cohort.
METHODS METHODS
We collected sebum by oil-blotting film of infants aged 1 and 2 months and analysed RNAs in their sebum. We diagnosed AD according to the United Kingdom Working Party's criteria.
RESULTS RESULTS
Infants with AD aged 1 month showed lower expression of genes related to various lipid metabolism and synthesis, antimicrobial peptides, tight junctions, desmosomes and keratinization. They also had higher expression of several genes involved in Th2-, Th17- and Th22-type immune responses and lower expression of negative regulators of inflammation. In addition, gene expressions related to innate immunity were higher in AD infants. Infants aged 1 month with neonatal acne and diagnosed with AD aged 2 months already had gene expression patterns similar to AD aged 1 month in terms of redox, lipid synthesis, metabolism and barrier-related gene expression.
CONCLUSION CONCLUSIONS
We identified molecular changes in barrier function and inflammatory markers that characterize the pathophysiology of AD in infants aged 1 month. We also revealed that neonatal acne at 1 month could predict the subsequent development of AD by sebum transcriptome data.

Identifiants

pubmed: 36897437
doi: 10.1111/jdv.19017
doi:

Substances chimiques

RNA, Messenger 0
RNA 63231-63-0
Lipids 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1385-1395

Subventions

Organisme : Japan Agency for Medical Research and Development
ID : JP22he0422021j0001
Organisme : Kao Corporation

Informations de copyright

© 2023 The Authors. Journal of the European Academy of Dermatology and Venereology published by John Wiley & Sons Ltd on behalf of European Academy of Dermatology and Venereology.

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Auteurs

Kiwako Yamamoto-Hanada (K)

Allergy Center, National Center for Child Health and Development, Tokyo, Japan.

Mayako Saito-Abe (M)

Allergy Center, National Center for Child Health and Development, Tokyo, Japan.

Kyoko Shima (K)

Biological Science Research, Kao Corporation, Tochigi, Japan.

Satoko Fukagawa (S)

Biological Science Research, Kao Corporation, Tochigi, Japan.

Yuya Uehara (Y)

Biological Science Research, Kao Corporation, Tochigi, Japan.

Yui Ueda (Y)

Biological Science Research, Kao Corporation, Tochigi, Japan.

Maeko Iwamura (M)

Biological Science Research, Kao Corporation, Tochigi, Japan.

Takatoshi Murase (T)

Biological Science Research, Kao Corporation, Tochigi, Japan.

Tetsuya Kuwano (T)

Biological Science Research, Kao Corporation, Tochigi, Japan.

Takayoshi Inoue (T)

Biological Science Research, Kao Corporation, Tochigi, Japan.

Yukihiro Ohya (Y)

Allergy Center, National Center for Child Health and Development, Tokyo, Japan.

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