Light-emitting diodes downregulate cathelicidin, kallikrein and toll-like receptor 2 expressions in keratinocytes and rosacea-like mouse skin

Abstract Cathelicidin ( LL ‐37), Toll‐like receptor 2 ( TLR ‐2) and kallikreins ( KLK s) 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 ( LED s) on LL ‐37, KLK s, TLR ‐2 and protease activity in cultured normal human epidermal keratinocytes ( NHEK s) and rosacea‐like mouse skin ( RLMS ). LL ‐37, KLK 5, KLK 7 and vitamin D receptor were induced by 1α, 25‐dihydroxyvitamin D 3 ( VD 3 ) and TLR ‐2 by Ad‐ CMV transfection in cultured NHEK s. NHEK s were subjected to LED irradiation at differing wavelengths (480–940 nm) and fluences (1–40 J/cm 2 ). Inflammatory mediators were analysed with RT ‐ PCR and real‐time PCR and protease activity analysis and immunocytofluorescence staining were performed for NHEK s. Changes in RLMS induced by LL ‐37 peptide were evaluated with real‐time PCR , immunohistochemical staining and enzyme‐linked immunosorbent assay. In NHEK s, LED at 630 and 940 nm significantly attenuated LL 37, 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 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, KLK 5 and LL ‐37 expressions and protease activity in NHEK and RLMS . Thus, LED s may be promising for rosacea treatment. However, clinical trials are required for further study.