Effects of blue light on inflammation and skin barrier recovery following acute perturbation. Pilot study results in healthy human subjects.

BACKGROUND/PURPOSE: While growing evidence supports the therapeutic effect of 453 nm blue light in chronic inflammatory skin diseases, data on its effects on acutely perturbed human skin are scarce. In this study, we investigated the impact of 453 nm narrow-band LED light on healthy skin following acute perturbation. METHODS: Tape stripping and histamine iontophoresis were performed on the forearm of 22 healthy volunteers on 2 consecutive weeks. In 1 week, challenges were followed by irradiation for 30 minutes. In the other week (control), no light was administered. Reactions were evaluated up to 72 hours thereafter by transepidermal water loss (TEWL), diffuse reflectance spectroscopy, and skin surface biomarkers. RESULTS: Skin barrier disruption resulted in upregulation of IL-1α at 24 hours after tape stripping (P = .029). In contrast, irradiation abrogated this effect (P > .05). Irradiation also resulted in higher TEWL at 24 hours and in higher b* value at 72 hours after tape stripping compared to the control (P = .034 and P = .018, respectively). At 30 minutes following histamine iontophoresis and irradiation, a trend toward a higher a* value compared to the control was observed (P = .051). CONCLUSION: We provide the first in vivo evidence that blue light at 453 nm exerts biological effects on acutely perturbed healthy human skin.

Gene expression profiling reveals aryl hydrocarbon receptor as a possible target for photobiomodulation when using blue light.

Photobiomodulation (PBM) with blue light induces a biphasic dose response curve in proliferation of immortalized human keratinocytes (HaCaT), with a maximum anti-proliferative effect reached with 30min (41.4 J/cm2). The aim of this study was to test the photobiomodulatory effect of 41.4 J/cm2 blue light irradiation on ROS production, apoptosis and gene expression at different time points after irradiation of HaCaT cells in vitro and assess its safety. ROS concentration was increased 30 min after irradiation. However, already 1 h after irradiation, cells were able to reduce ROS and balance the concentration to a normal level. The sudden increase in ROS did not damage the cells, which was demonstrated with FACS analysis where HaCaT cells did not show any sign of apoptosis after blue light irradiation. Furthermore, a time course could be seen in gene expression analysis after blue light, with an early response of stimulated genes already 1 h after blue light irradiation, leading to the discovery of the aryl hydrocarbon receptor as possible target for blue light irradiation.