Non-thermal atmospheric plasma ameliorates imiquimod-induced psoriasis-like skin inflammation in mice through inhibition of immune responses and up-regulation of PD-L1 expression.

Abstract

Abstract Plasma medicine is emerging as a novel therapeutic field. It has been reported that plasma can kill bacteria, promote wound healing and induce apoptosis of tumor cells. However, the effects of plasma on immune cells and immune related skin diseases have not been well studied. In this study, we demonstrated that non-thermal atmospheric plasma (NTP) treatment can inhibit psoriasis-like skin inflammation in mice. Psoriasis-like skin inflammation was induced through application of imiquimod for 5 days and NTP was treated on days 3 and 4. On day 5 mice were sacrificed for analysis. NTP treatment in imiquimod-applied mouse skin inhibited increases in epithelial cell thickness compared to imiquimod-applied mouse skin without NTP treatment and suppressed immune cell infiltration in the mouse skins. The expression of cytokines and chemokines and NF-κB activation in the skin were also suppressed by the NTP treatment. In addition, differentiation of Th17 cells, an important cell type for the pathogenesis of psoriasis, was inhibited in the NTP-treated mouse lymph nodes. It was also demonstrated that liquid type plasma (LTP), which is also known as indirect plasma, inhibited Th17 cell differentiation in vitro. Other in vitro experiments showed that LTP inhibits bone marrow-derived dendritic cell (BMDC) activation, and inflammation of HaCaT cells. Interestingly, LTP enhanced PD-L1 expression in BMDC and HaCaT cells, suggesting that NTP may inhibit unwanted over-activation of T cells through increased PD-L1 expression in dendritic cells or epithelial cells. Taken together, these results suggest that NTP can be used to treat CD4+ T cell-mediated autoimmune diseases such as psoriasis.