Expression of Periostin in Normal, Atopic, and Nonatopic Chronically Inflamed Canine Skin

Abstract

In humans, periostin plays a critical role in the enhancement and chronicity of allergic skin inflammation; however, whether it is involved in the pathogenesis of canine dermatitis remains unknown. The aim of this study was to examine the expression patterns of periostin in healthy, atopic, and nonatopic chronically inflamed canine skin. Biopsy specimens from 47 dogs with skin disease and normal skin tissue from 5 adult beagles were examined by light microscopy, immunohistochemistry, and in situ hybridization. In normal skin, periostin was localized just beneath the epidermis and around the hair follicles. In chronically inflamed skin, periostin expression was most intense in the dermis with inflammatory cell infiltrates. In contrast, low levels of periostin were detected in acutely inflamed and noninflamed skin. Conversely, all canine atopic dermatitis tissues characteristically showed the most intense expression of periostin in the superficial dermis, particularly at the epidermal-dermal junction. In situ hybridization showed that periostin mRNA was broadly expressed in the basal epidermal keratinocytes, outer root sheath cells, and dermal fibroblasts in normal dog skin. High expression of periostin mRNA was observed in fibroblasts in dog skin with chronically inflamed dermatitis. Moreover, in some chronically inflamed skin specimens, periostin mRNA expression was increased in basal keratinocytes. The severity score of chronic pathologic changes and CD3+ cell number in the dermis were correlated with distribution pattern of periostin in the atopic skin. These data suggest that periostin could play a role in the pathophysiology of chronic dermatitis, including atopic dermatitis, in dogs.

A study on periostin involvement in the pathophysiology of canine atopic skin

“…We have previously reported that PO expression was more intense in the canine atopic dermis and correlated with the severity of chronic histopathological lesions (epidermal thickening and fibrosis) and CD3+ cell number in the dermis, similar to these reported in hAD patients [ 15 ]. In the article, in situ hybridization (ISH) showed that fibroblasts and keratinocytes were the main source of PO in cAD [ 15 ]. These results suggested that PO may be involved in the pathogenesis of chronicity in cAD.…”

“…Double-ISH for PO and IL-13/ TGF-β1 was performed using the QuantiGene® ViewRNA ISH Tissue Assay (Affymetrix, Santa Clara, CA, U.S.A.) according to the manufacturer’s protocol, as described previously [ 15 ]. Type 1/Fast Red was used for PO probes and Type 6/Fast Blue was applied for IL-13 and TGF-β1.…”

“…Double-ISH sections were counterstained with Mayer’s hematoxylin. To identify the expressing IL-13 mRNA on CD3 positive cells, serial sections were additionally subjected to IHC for CD3 (rabbit anti–human CD3; Dako Denmark A/S., Glostrup, Denmark) as previously described [ 15 ]. An ISH reaction solution without the probes was used as a negative control, according to the manufacturer’s recommendations.…”

“…Previous studies have reported that cytokines and chemokines such as thymus and activation-regulated chemokine (TARC/CCL17) are exclusively produced by keratinocytes in human and canine atopic skin [ 12 ]. From our previous results [ 15 ], we assumed that PO may involve in epidermal thickening and the infiltration of inflammatory cells, which are major pathologic features in atopic skin.…”

Periostin as a multifunctional modulator of the wound healing response

“…The role of Postn in skin pathologies (Arima, et al, 2015, Crawford, et al, 2015, Mineshige, et al, 2015, Shiraishi, et al, 2012, Song and Qin, 2008, Supp, et al, 2012, Yamaguchi, et al, 2013, Zhang, et al, 2015, Zhou, et al, 2010) and wound healing (Elliott, et al, 2012a, Elliott, et al, 2012b, Jackson-Boeters, et al, 2009, Nishiyama, et al, 2011, Ontsuka, et al, 2012, Walker, et al, 2015, Zhou, et al, 2010) has been the subject of intense research, which has pointed to very specific roles for Postn.…”