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Zimmer, Béla; Angioni, Carlo; Osthues, Tabea; Toewe, Andy; Thomas, Dominique; Pierre, Sandra C.; Geisslinger, Gerd; Scholich, Klaus; Sisignano, Marco
Biochimica et biophysica acta. Molecular and cell biology of lipids, July 2018, 2018-07-00, 20180701, Letnik: 1863, Številka: 7Journal Article
Eicosanoids play a crucial role in inflammatory pain. However, there is very little knowledge about the contribution of oxidized linoleic acid metabolites in inflammatory pain and peripheral sensitization. Here, we identify 12,13-dihydroxy-9Z-octadecenoic acid (12,13-DiHOME), a cytochrome P450-derived linoleic acid metabolite, as crucial mediator of thermal hyperalgesia during inflammatory pain. We found 12,13-DiHOME in increased concentrations in peripheral nervous tissue during acute zymosan- and complete Freund's Adjuvant-induced inflammatory pain. 12,13-DiHOME causes calcium transients in sensory neurons and sensitizes the transient receptor potential vanilloid 1 (TRPV1)-mediated intracellular calcium increases via protein kinase C, subsequently leading to enhanced TRPV1-dependent CGRP-release from sensory neurons. Peripheral injection of 12,13-DiHOME in vivo causes TRPV1-dependent thermal pain hypersensitivity. Finally, application of the soluble epoxide hydrolase (sEH)-inhibitor TPPU reduces 12,13-DiHOME concentrations in nervous tissue and reduces zymosan- and CFA-induced thermal hyperalgesia in vivo. In conclusion, we identify a novel role for the lipid mediator 12,13-DiHOME in mediating thermal hyperalgesia during inflammatory pain and propose a novel mechanism that may explain the antihyperalgesic effects of sEH inhibitors in vivo. •The concentrations of the oxidized lipid 12,13-DiHOME increase during inflammatory pain.•12,13-DiHOME induces thermal pain hypersensitivity via TRPV1.•The sEH-inhibitor TPPU reduces DiHOME concentrations in nervous tissue in vivo.•TPPU reduces both CFA- and zymosan-induced thermal hyperalgesia in vivo.•A novel mechanism of how sEH-inhibition reduces thermal hyperalgesia is proposed.
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