Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis

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  • Arima Kazuhiko
    Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School
  • Ohta Shoichiro
    Department of Laboratory Medicine, Saga Medical School
  • Takagi Atsushi
    Department of Dermatology, Juntendo University of School of Medicine
  • Shiraishi Hiroshi
    Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School
  • Masuoka Miho
    Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School
  • Ontsuka Kanako
    Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School
  • Suto Hajime
    Atopy Research Center, Juntendo University of School of Medicine
  • Suzuki Shoichi
    Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School
  • Yamamoto Ken-ichi
    Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School
  • Ogawa Masahiro
    Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School
  • Simmons Olga
    Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine
  • Yamaguchi Yukie
    Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine
  • Toda Shuji
    Department of Pathology and Biodefense, Saga Medical School
  • Aihara Michiko
    Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine
  • Conway Simon J.
    Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine
  • Ikeda Shigaku
    Department of Dermatology, Juntendo University of School of Medicine
  • Izuhara Kenji
    Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School

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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.<br>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).<br>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.<br>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.

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