Ultraviolet light-emitting-diode irradiation inhibits TNF-α and IFN-γ-induced expression of ICAM-1 and STAT1 phosphorylation in human keratinocytes

Lasers Surg Med. 2015 Dec;47(10):824-32. doi: 10.1002/lsm.22425. Epub 2015 Sep 28.

Abstract

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.

Keywords: HaCaT; UV-LEDs; atopic dermatitis.

Publication types

  • Evaluation Study

MeSH terms

  • Biomarkers / metabolism
  • Blotting, Western
  • Cell Line
  • Enzyme-Linked Immunosorbent Assay
  • Fibroblasts / metabolism
  • Fibroblasts / radiation effects
  • Humans
  • Immunohistochemistry
  • Intercellular Adhesion Molecule-1 / metabolism*
  • Interferon-gamma / metabolism*
  • Keratinocytes / metabolism
  • Keratinocytes / radiation effects*
  • Phosphorylation / radiation effects*
  • Reverse Transcriptase Polymerase Chain Reaction
  • STAT1 Transcription Factor / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism*
  • Ultraviolet Rays*
  • Ultraviolet Therapy / instrumentation

Substances

  • Biomarkers
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • Interferon-gamma