Parachlorella beijerinckii-derived carotenoids ameliorate inflammation in a psoriasis-like mouse model via modulation of pro-inflammatory cytokines in dendritic cells.

Psoriasis is one of the most common chronic inflammatory skin diseases. Many studies suggest that dendritic cells (DCs) and the T cell-mediated interleukin (IL)-23/IL-17 axis play a central role in the signaling pathway in the pathogenesis of psoriasis. Chlorella, also known as Parachlorella beijerinckii (PB), is a unicellular green alga that has long been used as a health food. It contains carotenoids that have antioxidant and anti-inflammatory effects. In this study, we investigated whether PB-derived carotenoids (PBCs) ameliorated inflammatory processes in an imiquimod (IMQ)-induced psoriasis-like mouse model and bone marrow-derived dendritic cells (BMDCs). We found that PBCs attenuated erythema, thickness, scaling, and neutrophil infiltration in the skin tissue of the IMQ-induced psoriasis-like mice. Moreover, PBCs suppressed psoriasis-related pro-inflammatory cytokine expression, DC activation, and IL-17A production by γδ T cells in IMQ-induced psoriasis-like mice. In IMQ-induced BMDCs, PBCs suppressed the expression levels of pro-inflammatory cytokines, including IL-23; IL-1β; and IL-6; and CD40/CD86, a marker of DC activation. Additionally, PBCs inhibited the nuclear factor kappa B, p38, and c-Jun NH2-terminal kinase inflammatory signaling pathways and the mitochondrial reactive oxygen species (mitoROS)-triggered inflammasome activation pathway. PBCs also activated the extracellular regulated protein kinase/NF-E2-related factor-2 (ERK/Nrf2) pathway in BMDCs. Moreover, PBCs suppressed the harmful effects of pro-inflammatory cytokine gene expression and mitoROS and inflammasome activation via ERK/Nrf2 pathway activation in IMQ-induced BMDCs. In conclusion, PBCs may be beneficial in the management of psoriatic inflammation.