Cell type-dependent effects of corticosteroid on periostin production by primary human tissue cells

Authors

  • T. Shoda,

    1. Department of Health and Psychosocial Medicine, Aichi Medical University School of Medicine, Aichi
    2. Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan
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  • K. Futamura,

    1. Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan
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  • F. Kobayashi,

    1. Department of Health and Psychosocial Medicine, Aichi Medical University School of Medicine, Aichi
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  • H. Saito,

    1. Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan
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  • K. Matsumoto,

    1. Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan
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  • A. Matsuda

    Corresponding author
    1. Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan
    • Correspondence

      Akio Matsuda, PhD, Department of Allergy and Immunology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, 157-8535 Tokyo, Japan.

      Tel.: +81-3-5494-7120 ext. 4955

      Fax: +81-3-5494-7173

      E-mail: matsuda-a@ncchd.go.jp

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  • T.S. and K.F. contributed equally to this work.
  • Edited by: Michael Wechsler

Abstract

Overproduction of periostin, an IL-13-inducible matricellular protein, despite corticosteroid treatment is thought to be involved in the chronicity of allergic inflammation seen in corticosteroid-refractory tissue fibrosis. Therefore, we hypothesized that some tissue cells must produce periostin in a corticosteroid-insensitive manner. Here, we show that IL-4 and IL-13 each induced comparable levels of periostin production by primary normal human fibroblasts and microvascular endothelial cells derived from lung and skin. Dexamethasone, a corticosteroid, completely inhibited IL-4/13-induced, but did not affect TGF-β-induced, periostin production by fibroblasts. In contrast, dexamethasone synergistically enhanced IL-4/13-induced periostin production by microvascular endothelial cells. TGF-β did not induce periostin production by microvascular endothelial cells. Our novel findings suggest that IL-4/13-induced microvascular endothelium-derived and/or TGF-β-induced fibroblast-derived periostin might play a pivotal role in corticosteroid-refractory tissue fibrosis, leading to chronic allergic inflammation in the lung and/or skin.

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