Kazuhiko Arima1, Shoichiro Ohta2, Atsushi Takagi3, Hiroshi Shiraishi1, Miho Masuoka1, Kanako Ontsuka1, Hajime Suto4, Shoichi Suzuki1, Ken-Ichi Yamamoto1, Masahiro Ogawa1, Olga Simmons5, Yukie Yamaguchi6, Shuji Toda7, Michiko Aihara6, Simon J Conway5, Shigaku Ikeda3, Kenji Izuhara8. 1. Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan. 2. Department of Laboratory Medicine, Saga Medical School, Saga, Japan. 3. Department of Dermatology, Juntendo University of School of Medicine, Tokyo, Japan. 4. Atopy Research Center, Juntendo University of School of Medicine, Tokyo, Japan. 5. Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA. 6. Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan. 7. Department of Pathology and Biodefense, Saga Medical School, Saga, Japan. 8. Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan. Electronic address: kizuhara@cc.saga-u.ac.jp.
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.
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 psoriasispatients, 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 psoriasismouse model induced by topical treatment with imiquimod (IMQ). RESULTS:Periostin was substantially expressed in the dermis of all investigated psoriasispatients. Epidermal hyperplasia induced by IMQ treatment was impaired in periostin-deficient mice, along with decreased skin swelling. However, upon treatment with IMQ, periostindeficiency 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.
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