Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis

Kazuhiko Arima, Shoichiro Ohta, Atsushi Takagi, Hiroshi Shiraishi, Miho Masuoka, Kanako Ontsuka, Hajime Suto, Shoichi Suzuki, Ken Ichi Yamamoto, Masahiro Ogawa, Olga Simmons, Yukie Yamaguchi, Shuji Toda, Michiko Aihara, Simon Conway, Shigaku Ikeda, Kenji Izuhara

Research output: Contribution to journalArticle

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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.

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.

Original languageEnglish (US)
Pages (from-to)41-48
Number of pages8
JournalAllergology International
Volume64
Issue number1
DOIs
StatePublished - Jan 1 2015

Fingerprint

imiquimod
Atopic Dermatitis
Psoriasis
Hyperplasia
Interleukin-17
Skin
Interleukin-23
Immune System Diseases
Dermis
Coculture Techniques
Neutrophils
Therapeutics
Lymphocytes
Inflammation
Biopsy
interleukin-22
Proteins

Keywords

  • Epidermis
  • Hyperplasia
  • Imiquimod
  • Periostin
  • Psoriasis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Arima, K., Ohta, S., Takagi, A., Shiraishi, H., Masuoka, M., Ontsuka, K., ... Izuhara, K. (2015). Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis. Allergology International, 64(1), 41-48. https://doi.org/10.1016/j.alit.2014.06.001

Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis. / Arima, Kazuhiko; Ohta, Shoichiro; Takagi, Atsushi; Shiraishi, Hiroshi; Masuoka, Miho; Ontsuka, Kanako; Suto, Hajime; Suzuki, Shoichi; Yamamoto, Ken Ichi; Ogawa, Masahiro; Simmons, Olga; Yamaguchi, Yukie; Toda, Shuji; Aihara, Michiko; Conway, Simon; Ikeda, Shigaku; Izuhara, Kenji.

In: Allergology International, Vol. 64, No. 1, 01.01.2015, p. 41-48.

Research output: Contribution to journalArticle

Arima, K, Ohta, S, Takagi, A, Shiraishi, H, Masuoka, M, Ontsuka, K, Suto, H, Suzuki, S, Yamamoto, KI, Ogawa, M, Simmons, O, Yamaguchi, Y, Toda, S, Aihara, M, Conway, S, Ikeda, S & Izuhara, K 2015, 'Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis', Allergology International, vol. 64, no. 1, pp. 41-48. https://doi.org/10.1016/j.alit.2014.06.001
Arima, Kazuhiko ; Ohta, Shoichiro ; Takagi, Atsushi ; Shiraishi, Hiroshi ; Masuoka, Miho ; Ontsuka, Kanako ; Suto, Hajime ; Suzuki, Shoichi ; Yamamoto, Ken Ichi ; Ogawa, Masahiro ; Simmons, Olga ; Yamaguchi, Yukie ; Toda, Shuji ; Aihara, Michiko ; Conway, Simon ; Ikeda, Shigaku ; Izuhara, Kenji. / Periostin contributes to epidermal hyperplasia in psoriasis common to atopic dermatitis. In: Allergology International. 2015 ; Vol. 64, No. 1. pp. 41-48.
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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.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.",
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AU - Arima, Kazuhiko

AU - Ohta, Shoichiro

AU - Takagi, Atsushi

AU - Shiraishi, Hiroshi

AU - Masuoka, Miho

AU - Ontsuka, Kanako

AU - Suto, Hajime

AU - Suzuki, Shoichi

AU - Yamamoto, Ken Ichi

AU - Ogawa, Masahiro

AU - Simmons, Olga

AU - Yamaguchi, Yukie

AU - Toda, Shuji

AU - Aihara, Michiko

AU - Conway, Simon

AU - Ikeda, Shigaku

AU - Izuhara, Kenji

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N2 - 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.

AB - 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.

KW - Epidermis

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KW - Psoriasis

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