Therapeutic Effects of Full Spectrum Light on the Development of Atopic Dermatitis‐like Lesions in NC/Nga Mice. (19th May 2014)

• Record Type: Journal Article
• Authors: Kwon, Tae‐Rin; Mun, Seog Kyun; Oh, Chang Taek; Hong, Hyuckki; Choi, Yeon Shik; Kim, Bong‐Jun; Kim, Beom Joon
• Is Part Of: Photochemistry and photobiology. Volume 90:Number 5(2014:Sep./Oct.)
• Page Start: 1160
• Page End: 1169
• Publication Date: 2014-05-19
• Subjects: Photochemistry -- Periodicals; Light -- Physiological effect -- Periodicals; 541.35
• DOI: 10.1111/php.12284
• Languages: English
• ISSNs: 0031-8655

Abstract

<abstract abstract-type="main" id="php12284-abs-0001"> <title>Abstract</title> <p>Full spectrum light (FSL) includes UVA, visible light and infrared light. Many studies have investigated the application of FSL in severe cases of atopic dermatitis (AD) in humans; however, FSL has not yet been studied in an animal model. The purpose of this study was to evaluate the therapeutic effects of FSL on AD‐like skin lesions using NC/Nga mice, with the aim of mitigating itching and attenuating the expression of adhesion molecules. We examined the effects of FSL on mite allergen‐treated NC/Nga mice by assessing skin symptom severity, ear thickness, serum IgE levels, and the cytokine expression. We examined the histology of lesions using hematoxylin–eosin, toluidine blue and immunohistochemical staining. Our findings suggest that FSL phototherapy exerts positive therapeutic effects on <italic>Dermatophagoides farinae</italic> (Df)‐induced AD‐like skin lesions in NC/Nga mice by reducing IgE levels, thus promoting recovery of the skin barrier. The mechanisms by which FSL phototherapy exerts its effects may also involve the inhibition of scratching behavior, reduction of IL‐6 levels and reductions in adhesion molecule expression. The present study indicates that FSL phototherapy inhibits the development of AD in NC/Nga mice by suppressing cytokine, chemokine and adhesion molecule expression, and thus, could potentially be useful in treating AD.</p> </abstract>