title: Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis.
abstract: BACKGROUND
  Epidermal hyperplasia is a histological hallmark observed in both atopic dermatitis (AD) and psoriasis, although the clinical features and the underlying immunological disorders of these diseases are different. We previously showed that periostin, a matricellular protein, plays a critical role in epidermal hyperplasia in AD, using a mouse model and a 3-dimensional organotypic coculture system. In this study, we explore the hypothesis that periostin is involved in epidermal hyperplasia in psoriasis.
  
  
  METHODS
  To examine expression of periostin in psoriasis patients, we performed immunohistochemical analysis on skin biopsies from six such patients. To investigate periostin's role in the pathogenesis of psoriasis, we evaluated periostin-deficient mice in a psoriasis mouse model induced by topical treatment with imiquimod (IMQ).
  
  
  RESULTS
  Periostin was substantially expressed in the dermis of all investigated psoriasis patients. Epidermal hyperplasia induced by IMQ treatment was impaired in periostin-deficient mice, along with decreased skin swelling. However, upon treatment with IMQ, periostin deficiency did not alter infiltration of inflammatory cells such as neutrophils; production of IL-17, -22, or -23; or induction/expansion of IL-17- and IL-22-producing group 3 innate lymphoid cells.
  
  
  CONCLUSIONS
  Periostin plays an important role during epidermal hyperplasia in IMQ-induced skin inflammation, independently of the IL-23-IL-17/IL-22 axis. Periostin appears to be a mediator for epidermal hyperplasia that is common to AD and psoriasis.
authors.affiliation: Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Arima
authors.affiliation: Department of Laboratory Medicine, Saga Medical School, Saga, Japan.
authors.forename: Shoichiro
authors.initials: S
authors.lastname: Ohta
authors.affiliation: Department of Dermatology, Juntendo University of School of Medicine, Tokyo, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Takagi
authors.affiliation: Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Shiraishi
authors.affiliation: Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
authors.forename: Miho
authors.initials: M
authors.lastname: Masuoka
authors.affiliation: Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
authors.forename: Kanako
authors.initials: K
authors.lastname: Ontsuka
authors.affiliation: Atopy Research Center, Juntendo University of School of Medicine, Tokyo, Japan.
authors.forename: Hajime
authors.initials: H
authors.lastname: Suto
authors.affiliation: Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
authors.forename: Shoichi
authors.initials: S
authors.lastname: Suzuki
authors.affiliation: Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Yamamoto
authors.affiliation: Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Ogawa
authors.affiliation: Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.
authors.forename: Olga
authors.initials: O
authors.lastname: Simmons
authors.affiliation: Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
authors.forename: Yukie
authors.initials: Y
authors.lastname: Yamaguchi
authors.affiliation: Department of Pathology and Biodefense, Saga Medical School, Saga, Japan.
authors.forename: Shuji
authors.initials: S
authors.lastname: Toda
authors.affiliation: Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
authors.forename: Michiko
authors.initials: M
authors.lastname: Aihara
authors.affiliation: Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.
authors.forename: Simon J
authors.initials: SJ
authors.lastname: Conway
authors.affiliation: Department of Dermatology, Juntendo University of School of Medicine, Tokyo, Japan.
authors.forename: Shigaku
authors.initials: S
authors.lastname: Ikeda
authors.affiliation: Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan. Electronic address: kizuhara@cc.saga-u.ac.jp.
authors.forename: Kenji
authors.initials: K
authors.lastname: Izuhara
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D001706:Biopsy; D015815:Cell Adhesion Molecules / Q000235:genetics* / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000235:genetics* / Q000276:immunology / Q000473:pathology*; D004195:Disease Models, Animal; D004817:Epidermis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D015870:Gene Expression; D006801:Humans; D006965:Hyperplasia; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000378:metabolism; D016131:Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008875:Middle Aged; D011565:Psoriasis / Q000235:genetics* / Q000276:immunology / Q000473:pathology*; D012867:Skin / Q000276:immunology / Q000378:metabolism / Q000473:pathology
chemical_list: D015815:Cell Adhesion Molecules; D016207:Cytokines; D018836:Inflammation Mediators; C512835:POSTN protein, human
keywords: Epidermis; Hyperplasia; Imiquimod; Periostin; Psoriasis