Journal
ALLERGOLOGY INTERNATIONAL
Volume 64, Issue 1, Pages 41-48Publisher
JAPANESE SOCIETY ALLERGOLOGY
DOI: 10.1016/j.alit.2014.06.001
Keywords
Epidermis; Hyperplasia; Imiquimod; Periostin; Psoriasis
Categories
Funding
- Japan Society for the Promotion of Science
- Riley Children's Foundation
- National Institutes of Health
- Grants-in-Aid for Scientific Research [24591468, 25293224, 15K15372, 15K09553] Funding Source: KAKEN
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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. Copyright (C) 2014, Japanese Society of Allergology. Production and hosting by Elsevier B.V. All rights reserved.
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