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Ultraviolet B eye irradiation aggravates atopic dermatitis via adrenocorticotropic hormone and NLRP 3 inflammasome in NC /Nga mice
Author(s) -
Hiramoto Keiichi,
Yamate Yurika,
Yokoyama Satoshi
Publication year - 2018
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/phpp.12372
Subject(s) - inflammasome , adrenocorticotropic hormone , pyrin domain , irradiation , thymic stromal lymphopoietin , caspase 1 , atopic dermatitis , nalp3 , receptor , medicine , immunology , chemistry , hormone , endocrinology , inflammation , physics , nuclear physics
Summary Background Ultraviolet ( UV ) B irradiation has been shown to improve atopic dermatitis ( AD ). However, the relationship between UVB eye irradiation and AD is not known. This issue was addressed using a mouse model of AD . Methods The eyes of NC /Nga mice were irradiated with UVB at a dose of 1.0 kJ /m 2 using a 20 SE sunlamp for the duration of the experimental period. Results AD symptoms deteriorated upon UVB eye irradiation. The levels of adrenocorticotropic hormone ( ACTH ) in the plasma and nucleotide‐binding domain and leucine‐rich‐containing family, pyrin domain‐containing ( NLRP )3 and neutrophil markers in the skin were increased in UVB ‐irradiated mice. Treatment with inhibitors of ACTH , caspase‐1, interleukin‐18, and thymic stromal lymphopoietin ( TSLP ) partly reversed the effects of irradiation, with the greatest improvement observed upon ACTH inhibition. The NLRP 3 inflammasome was implicated in the effects of UVB irradiation. Conclusions UVB eye irradiation causes AD symptom deterioration, which is likely mediated by ACTH and the activity of the inflammasome.