Abstract
Several studies suggest that light in the UVA range (320-400 nm) activates signaling pathways that are anti-inflammatory and antioxidative. These effects have been attributed to Nrf2-mediated upregulation of "phase 2" genes such as heme oxygenase-1 (HO-1) that neutralize oxidative stress and metabolize electrophiles. Proteomics analysis previously had shown that small doses of blue light (400-500 nm) increased levels of peroxiredoxin phase 2 proteins in THP-1 monocytes, which led to our hypothesis that blue light activates Nrf2 signaling and thus may serve as an anti-inflammatory agent. THP-1 monocytes were treated with doses of blue light with and without lipopolysaccharide (LPS) inflammatory challenge. Cell lysates were tested for Nrf2 activation and HO-1 production. Treated cells were assessed for viability/mitochondrial activity via trypan blue exclusion and MTT assay, and secretion of two major pro-inflammatory cytokines, interleukin 8 (IL8) and tumor necrosis factor alpha (TNFα) was measured using ELISA. Blue light activated the phase 2 response in cultured THP-1 cells and was protective against LPS-induced cytotoxicity. Light pre-treatment also significantly reduced cytokine secretion in response to 0.1 μg ml-1 LPS, but had no anti-inflammatory effect at high LPS levels. This study is the first to report these effects using a light source that is approved for routine use on dental patients. Cellular responses to these light energies are worth further study and may provide therapeutic interventions for inflammation.