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Ultraviolet light-emitting-diode irradiation inhibits TNF-α and IFN-γ-induced expression of ICAM-1 and STAT1 phosphorylation in human keratinocytes
Background and Objectives Ultraviolet light‐emitting diodes (UV‐LEDs) are a novel light source for phototherapy. This research investigated the in vitro safety and efficacy of UV‐LEDs as a phototherapeutic device for atopic dermatitis (AD). Study Design/Materials and Methods Human keratinocytes and...
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Published in: | Lasers in surgery and medicine 2015-12, Vol.47 (10), p.824-832 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background and Objectives
Ultraviolet light‐emitting diodes (UV‐LEDs) are a novel light source for phototherapy. This research investigated the in vitro safety and efficacy of UV‐LEDs as a phototherapeutic device for atopic dermatitis (AD).
Study Design/Materials and Methods
Human keratinocytes and fibroblasts were irradiated by UV‐LEDs with a center wavelength of 310 and 340 nm. We examined the effects of UV‐LED irradiation on the suppression of TNF‐α/IFN‐γ‐induced activation of STAT1 and ICAM‐1 and on NF‐κB expression; we used the following methods: cell viability assay, reverse transcription‐polymerase chain reaction, enzyme‐linked immunosorbent assay, Western blotting, and immunocytochemistry.
Results
We observed anti‐inflammatory responses through the suppression of TNF‐α/IFN‐γ‐induced expression of TARC and MCP‐1/CCL2, IL‐1beta, IL‐6, and sICAM‐1 via blockage of ICAM‐1 activation and subsequent activation of STAT1 and NF‐κB. The results suggested that UV‐LED irradiation inhibited ICAM expression by suppressing TNF‐α/IFN‐γ‐induced NF‐κB activation in vitro.
Conclusion
We concluded that novel UV‐LED (310 and 340 nm) modalities were effective for the treatment of AD and may be promising for the treatment of inflammatory skin diseases. Lasers Surg. Med. 47:824–832, 2015. © 2015 Wiley Periodicals, Inc. |
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ISSN: | 0196-8092 1096-9101 |
DOI: | 10.1002/lsm.22425 |