Journal of Veterinary Medical Science
Online ISSN : 1347-7439
Print ISSN : 0916-7250
ISSN-L : 0916-7250
Pathology
A study on periostin involvement in the pathophysiology of canine atopic skin
Takayuki MINESHIGEJunichi KAMIIEGo SUGAHARAKinji SHIROTA
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JOURNAL FREE ACCESS

2018 Volume 80 Issue 1 Pages 103-111

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Abstract

Atopic dermatitis (AD) is a chronic, pruritic, and allergic skin disease in humans and animals, particularly dogs. Canine AD (cAD) has received attention as a spontaneous atopic animal model because domesticated dogs inhabit a human environment, and cAD shares several clinicopathological features with human AD (hAD). In hAD, periostin (PO) is suggested to play a critical role in the enhancement and chronicity of allergic skin inflammation; however, PO involvement in the pathogenesis of cAD is unknown. Here we aimed to clarify PO involvement in the pathophysiology of cAD and focused on the inducing factor and function of PO in canine atopic skin. Using double-labeled in situ hybridization (ISH), interleukin (IL)-13 mRNA-positive cells were detected near the keratinocytes and dermal fibroblasts expressing PO mRNA in atopic skin. Using an in vitro assay, IL-13 induced PO gene expression in both canine dermal fibroblasts and keratinocytes. PO enhanced in vitro growth of canine keratinocytes. Moreover, among PO-induced genes in cultured canine keratinocytes detected using a microarray, we identified IL-25 as a possible mediator in canine atopic skin. In addition, real time polymerase chain reaction (PCR) analysis revealed upregulation of IL-25 gene expression in PO-stimulated keratinocytes. These data suggest that IL-13 possibly derived from T helper 2 (Th2) cells stimulates PO production in both keratinocytes and fibroblasts, and then PO may play a critical role in the pathophysiology of cAD, particularly in the enhancement and chronicity of skin lesions via IL-25.

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© 2018 by the Japanese Society of Veterinary Science

この記事はクリエイティブ・コモンズ [表示 - 非営利 - 改変禁止 4.0 国際]ライセンスの下に提供されています。
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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