401 Endocannabinoid pathway in Atopic Dermatitis: results from an in vitro pilot study

Atopic Dermatitis (AD) is a multifactorial disease. Activated keratinocytes release proinflammatory cytokines that induce Th2 lymphocytes to produce key AD inflammatory microenvironment. The endocannabinoid system (ECS), including cannabinoid receptors, their endogenous ligands and the metabolic enzymes of these ligands, has recently been implicated in regulation various skin process, proliferation immuno-tolerance keratinocytes. Alterations some components ECS have hypothesized AD, but no studies exhaustively investigated role all members ECS. In this pilot study, we studied expression vitro model. HaCaT were cultured DMEM with 10% FBS. maturation was obtained by adding 1.8 mM CaCl2 every day for 7 days. On last day, cells treated IL-4+IL13+INFγ at 10 ng/mL each 24 hours develop mRNA following genes evaluated, using TaqMan Real Time PCR Technology: CB1, CB2, GPR55, TRPV1, PPARα, PPARγ, PPARδ, NAPE-PLD, FAAH, DAGLα, DAGLβ, MAGL. Relative quantification performed comparative ΔΔCt method. Regarding observed significant 2-fold increase PPARα (p=0.02) vs control keratinocytes; GPR55 PPARδ resulted more elevated diseased cells, although differences borderline significativity (p=0.06 p=0.07, respectively). A not reported PPARγ TRPV1 transcripts (p=0.31, p=0.11 p=0.22 With regard enzymes, showed higher levels FAAH MAGL lower NAPE-PLD (p=0.15, p=0.23, p=0.70, DAGLα (p=0.264) DAGLβ (p=0.687) similar between two conditions. Our preliminary finding demonstrated modulation pathway atopic dermatitis vitro, marked PPAR nuclear receptors.