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Experimental dermatology · Dec 2016
Light-emitting diodes downregulate cathelicidin, kallikrein and toll-like receptor 2 expressions in keratinocytes and rosacea-like mouse skin.
- Jee-Bum Lee, Soo Hyeon Bae, Ki Rang Moon, Eui Young Na, Sook Jung Yun, and Seung-Chul Lee.
- Department of Dermatology, Chonnam National University Medical School, Gwangju, South Korea.
- Exp. Dermatol. 2016 Dec 1; 25 (12): 956-961.
AbstractCathelicidin (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. We investigated the effects of light-emitting diodes (LEDs) on LL-37, KLKs, TLR-2 and protease activity in cultured normal human epidermal keratinocytes (NHEKs) and rosacea-like mouse skin (RLMS). LL-37, KLK5, KLK7 and vitamin D receptor were induced by 1α, 25-dihydroxyvitamin D3 (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 (1-40 J/cm2 ). 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. In NHEKs, LED at 630 and 940 nm significantly attenuated LL37, KLK5 and TLR-2 mRNA expressions. Protease activity was significantly suppressed at 630, 850 and 940 nm. In the RLMS, LL-37, KLK5 and PAR-2 mRNA expressions significantly decreased at 24 and 48 hours after LED irradiation was performed three times 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. LED at 630 and 940 nm downregulated TLR-2, KLK5 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.© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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