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Mild electrical stimulation with heat shock reduces inflammatory symptoms in the imiquimod‐induced psoriasis mouse model
Author(s) -
Tsurekawa Yu,
Morita Misaki,
Suico Mary Ann,
Moriuchi Masataka,
Nakano Yoshio,
Piruzyan Mariam,
Takada Masafumi,
Fukami Sanako,
Shuto Tsuyoshi,
Kai Hirofumi
Publication year - 2018
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13720
Subject(s) - imiquimod , psoriasis , inflammation , hacat , medicine , stimulation , immunology , s100a9 , immune system , keratinocyte , pharmacology , endocrinology , chemistry , in vitro , biochemistry
Abstract Psoriasis is a chronic skin disease caused by immune disorder. The chronic skin inflammation involves inflammatory molecules that are released from T lymphocytes and keratinocytes. Therefore, developing an anti‐inflammatory therapy that is suitable for long‐term treatment is needed. Electrical stimulation induces biological responses by modulating intracellular signaling pathways. Our previous studies showed that the optimized combination treatment of mild electrical stimulation ( MES , 0.1‐millisecond; ms, 55‐pulses per second; pps) and heat shock ( HS , 42°C) modulates inflammatory symptoms of metabolic disorders and chronic kidney disease in mice models and clinical trials. Here, we investigated the effect of MES + HS treatment on imiquimod‐induced psoriasis mouse model. Topical application of imiquimod cream (15 mg) to mice ear induced keratinocyte hyperproliferation and psoriasis‐like inflammation. In MES + HS ‐treated mice, imiquimod‐induced skin hyperplasia was significantly decreased. MES + HS treatment reduced the protein expression of IL ‐17A and the infiltration of CD 3‐positive cells in lesioned skin. In addition, MES + HS ‐treated mice had decreased mRNA expression level of antimicrobial molecules ( S100A8 and Reg3 γ) which aggravate psoriasis. In IL ‐17A‐stimulated HaCaT cells, MES + HS treatment significantly lowered the mRNA expression of aggravation markers ( S100A8 , S100A9 and β ‐defensin2 ). Taken together, our study suggested that MES + HS treatment improves the pathology of psoriasis via decreasing the expression of inflammatory molecules.