Kistner Katrin, Siklosi Norbert, Babes Alexandru, Khalil Mohammad, Selescu Tudor, Zimmermann Katharina, Wirtz Stefan, Becker Christoph, Neurath Markus F, Reeh Peter W, Engel Matthias A
Institute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsstr. 17, 91054 Erlangen, Germany.
University of Bucharest Department of Physiology, Faculty of Biology, Splaiul Independentei 91-95, 050095 Bucharest, Romania.
Sci Rep. 2016 Jun 30;6:28621. doi: 10.1038/srep28621.
We demonstrate a novel dual strategy against inflammation and pain through body-wide desensitization of nociceptors via TRPA1. Attenuation of experimental colitis by capsazepine (CPZ) has long been attributed to its antagonistic action on TRPV1 and associated inhibition of neurogenic inflammation. In contrast, we found that CPZ exerts its anti-inflammatory effects via profound desensitization of TRPA1. Micromolar CPZ induced calcium influx in isolated dorsal root ganglion (DRG) neurons from wild-type (WT) but not TRPA1-deficient mice. CPZ-induced calcium transients in human TRPA1-expressing HEK293t cells were blocked by the selective TRPA1 antagonists HC 030031 and A967079 and involved three cysteine residues in the N-terminal domain. Intriguingly, both colonic enemas and drinking water with CPZ led to profound systemic hypoalgesia in WT and TRPV1(-/-) but not TRPA1(-/-) mice. These findings may guide the development of a novel class of disease-modifying drugs with anti-inflammatory and anti-nociceptive effects.
我们通过TRPA1使伤害感受器在全身范围内脱敏,展示了一种针对炎症和疼痛的新型双重策略。长期以来,辣椒素(CPZ)对实验性结肠炎的减轻作用一直归因于其对TRPV1的拮抗作用以及相关的神经源性炎症抑制。相比之下,我们发现CPZ通过使TRPA1深度脱敏发挥其抗炎作用。微摩尔浓度的CPZ在野生型(WT)而非TRPA1基因敲除小鼠的离体背根神经节(DRG)神经元中诱导钙内流。在表达人TRPA1的HEK293t细胞中,CPZ诱导的钙瞬变被选择性TRPA1拮抗剂HC 030031和A967079阻断,且涉及N端结构域中的三个半胱氨酸残基。有趣的是,用CPZ进行结肠灌肠和饮水均导致WT和TRPV1基因敲除小鼠出现深度全身性痛觉减退,但TRPA1基因敲除小鼠未出现。这些发现可能会指导一类具有抗炎和抗伤害感受作用的新型疾病改善药物的研发。