rss Posted June 18, 2016 Report Posted June 18, 2016 Light Emitting Diodes Down-regulates Cathelicidin, Kallikrein, and Toll-like Receptor 2 Expressions in Keratinocytes and Rosacea-like Mouse Skin. Exp Dermatol. 2016 Jun 17; Authors: Lee JB, Bae SH, Moon KR, Na EY, Yun SJ, Lee SC Abstract BACKGROUND: Cathelicidin (LL-37), Toll-like receptor 2 (TLR 2), and kallikreins (KLKs) are key inflammatory mediators in rosacea. Laser or light-based devices have been successfully used for rosacea. OBJECTIVE: We investigated the effects of light-emitting diodes (LED) on LL-37, KLKs, TLR 2, and protease activity in cultured normal human epidermal keratinocytes(NHEKs) and rosacea-like mouse skin(RLMS). METHODS: LL-37, KLK 5, KLK 7, and vitamin D receptor were induced by 1α,25-dihydroxyvitaminD3 (VD3 ) and TLR 2 by Ad-CMV transfection in cultured NHEKs. NHEKs were subjected to LED irradiation at differing wavelengths (480-940 nm) and fluences (1-80 40 J/cm(2) ). Inflammatory mediators were analysed with RT-PCR and real-time PCR and protease activity analysis and immunocytofluorescence staining were performed for NHEKs. Changes in RLMS induced by LL-37 peptide were evaluated with real time PCR, immunohistochemical staining, and enzyme linked immunosorbent assay. RESULTS: In NHEKs, LED at 630 and 940 nm significantly attenuated LL37, KLK 5 and TLR 2 mRNA expressions. Protease activity was significantly suppressed at 630, 850, and 940 nm. In the RLMS, LL-37, KLK 5, and PAR 2 mRNA expressions significantly decreased at 24 and 48 h after LED irradiation was performed three times thrice at 630 and 940 nm. mCAMP and IL-8 protein levels and protease activity after LED irradiation were lower than those in RLMS control groups. CONCLUSION: LED at 630 and 940 nm down-regulated TLR 2, KLK 5, and LL-37 expressions and protease activity in NHEK and RLMS. Thus, LEDs may be promising for rosacea treatment. However, clinical trials are required for further study. This article is protected by copyright. All rights reserved. PMID: 27315464 [PubMed - as supplied by publisher] {url} = URL to article
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