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lüll Protective role of palmitoylethanolamide in contact allergic dermatitis Petrosino S; Cristino L; Karsak M; Gaffal E; Ueda N; Tuting T; Bisogno T; De Filippis D; D'Amico A; Saturnino C; Orlando P; Zimmer A; Iuvone T; Di Marzo VAllergy 2010[Jun]; 65 (6): 698-711BACKGROUND: Palmitoylethanolamide (PEA) is an anti-inflammatory mediator that enhances the activation by anandamide (AEA) of cannabinoid receptors and transient receptor potential vanilloid type-1 (TRPV1) channels, and directly activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha). In mice, 2,4-dinitrofluorobenzene (DNFB)-induced contact allergic dermatitis (CAD) in inflamed ears is partly mediated by the chemokine Monocyte Chemotactic Protein-2 (MCP-2) and accompanied by elevation of AEA levels. No datum is available on PEA regulation and role in CAD. OBJECTIVE: We examined whether PEA is produced during DNFB-induced CAD, and if it has any direct protective action in keratinocytes in vitro. METHODS: Eight- to ten-week-old female C57BL/6J wild-type and CB(1)/CB(2) double knock-out mice were used to measure PEA levels and the expression of TRPV1, PPAR-alpha receptors and enzymes responsible for PEA biosynthesis and degradation. Human keratinocytes (HaCaT) cells were stimulated with polyinosinic polycytidylic acid [poly-(I:C)], and the expression and release of MCP-2 were measured in the presence of PEA and antagonists of its proposed receptors. RESULTS: 2,4-Dinitrofluorobenzene increased ear skin PEA levels and up-regulated TRPV1, PPAR-alpha and a PEA-biosynthesizing enzyme in ear keratinocytes. In HaCaT cells, stimulation with poly-(I:C) elevated the levels of both PEA and AEA, and exogenous PEA (10 microM) inhibited poly-(I:C)-induced expression and release of MCP-2 in a way reversed by antagonism at TRPV1, but not PPAR-alpha. PEA (5-10 mg/kg, intraperitoneal) also inhibited DNFB-induced ear inflammation in mice in vivo, in a way attenuated by TRPV1 antagonism. CONCLUSIONS: We suggest that PEA is an endogenous protective agent against DNFB-induced keratinocyte inflammation and could be considered for therapeutic use against CAD.|Amides[MESH]|Animals[MESH]|Anti-Inflammatory Agents, Non-Steroidal[MESH]|Anti-Inflammatory Agents/analysis[MESH]|Dermatitis, Allergic Contact/etiology/*metabolism[MESH]|Dinitrofluorobenzene[MESH]|Endocannabinoids[MESH]|Ethanolamines[MESH]|Female[MESH]|Inflammation/immunology[MESH]|Keratinocytes/metabolism/pathology[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Palmitic Acids/*analysis/immunology[MESH]|Protective Agents[MESH] |