Periostin activates distinct modules of inflammation and itching downstream of the type 2 inflammation pathway.


Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
31 01 2023
Historique:
received: 15 08 2022
revised: 06 11 2022
accepted: 15 12 2022
pubmed: 8 1 2023
medline: 7 2 2023
entrez: 7 1 2023
Statut: ppublish

Résumé

Atopic dermatitis (AD) is a chronic relapsing skin disease accompanied by recurrent itching. Although type 2 inflammation is dominant in allergic skin inflammation, it is not fully understood how non-type 2 inflammation co-exists with type 2 inflammation or how type 2 inflammation causes itching. We have recently established the FADS mouse, a mouse model of AD. In FADS mice, either genetic disruption or pharmacological inhibition of periostin, a downstream molecule of type 2 inflammation, inhibits NF-κB activation in keratinocytes, leading to downregulating eczema, epidermal hyperplasia, and infiltration of neutrophils, without regulating the enhanced type 2 inflammation. Moreover, inhibition of periostin blocks spontaneous firing of superficial dorsal horn neurons followed by a decrease in scratching behaviors due to itching. Taken together, periostin links NF-κB-mediated inflammation with type 2 inflammation and promotes itching in allergic skin inflammation, suggesting that periostin is a promising therapeutic target for AD.

Identifiants

pubmed: 36610396
pii: S2211-1247(22)01834-4
doi: 10.1016/j.celrep.2022.111933
pii:
doi:

Substances chimiques

NF-kappa B 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

111933

Informations de copyright

Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing financial interest.

Auteurs

Satoshi Nunomura (S)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan. Electronic address: nunomura@cc.saga-u.ac.jp.

Daisuke Uta (D)

Department of Applied Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan.

Isao Kitajima (I)

Department of Clinical Laboratory and Molecular Pathology, Graduate School of Medical and Pharmaceutical Science, University of Toyama, Toyama 930-0194, Japan.

Yasuhiro Nanri (Y)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.

Kosuke Matsuda (K)

Department of Applied Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan.

Naoko Ejiri (N)

Department of Clinical Laboratory and Molecular Pathology, Graduate School of Medical and Pharmaceutical Science, University of Toyama, Toyama 930-0194, Japan.

Midori Kitajima (M)

Department of Clinical Laboratory and Molecular Pathology, Graduate School of Medical and Pharmaceutical Science, University of Toyama, Toyama 930-0194, Japan.

Hitoshi Ikemitsu (H)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.

Misaki Koga (M)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.

Sayaka Yamamoto (S)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.

Yuko Honda (Y)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.

Hironobu Takedomi (H)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan.

Tsugunobu Andoh (T)

Department of Pharmacology and Pathophysiology, College of Pharmacy, Kinjo Gakuin University, Nagoya 463-8521, Japan.

Simon J Conway (SJ)

Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.

Kenji Izuhara (K)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, 5-1-1, Nabeshima, Saga 849-8501, Japan. Electronic address: kizuhara@cc.saga-u.ac.jp.

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Classifications MeSH