Abstract
Abstract Interleukin-27 (p28/EBI3) is expressed by activated antigen presenting cells in response to TLR ligands and pro-inflammatory cytokines. The immunosuppressive functions of IL-27 have previously been demonstrated to occur through the induction of type 1 regulatory T cells, inhibition of Th17 cell development, and anti-inflammatory effects in murine models of collagen-induced arthritis (CIA), inflammatory bowel disease (IBD), and experimental autoimmune encephalomyelitis. We previously showed the pro-inflammatory effects of PGE2 in CIA and IBD through stimulation of IL-23 production leading to development of Th17 cells. Here we report on a novel pro-inflammatory function of PGE2 through the inhibition of IL-27 production by LPS-stimulated and poly I:C-stimulated murine bone marrow-derived dendritic cells (BMDC) and macrophages. We determined the effect of PGE2 on LPS-stimulated BMDC was mediated through EP2/EP4 receptors and induction of cAMP. Previous studies detailed the involvement of NF-κB (c-Rel) and interferon regulatory factors in IL-27p28 gene activation. The current project examines the effect of PGE2 on c-Rel, IRF1 and IRF3 utilizing luciferase reporter assays, gene expression and protein analysis. These studies further characterize the inflammatory mechanisms of PGE2, and might identify novel therapeutic targets for treating inflammatory diseases.
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