چکیده (انگلیسی):

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-17e and IL-22eproducing group 3 innate lymphoid cells.
Conclusions: Periostin plays an important role during epidermal hyperplasia in IMQ-induced skin
inflammation, independently of the IL-23eIL-17/IL-22 axis. Periostin appears to be a mediator for
epidermal hyperplasia that is common to AD and psoriasis.