Anti‐inflammatory and immune‐regulatory mechanisms prevent contact hypersensitivity to Arnica montana L.
Anti‐inflammatory and immune‐regulatory mechanisms prevent contact hypersensitivity to Arnica montana L.
复制标题
抗炎和免疫调节机制可预防对山金车的接触过敏。
DOI：
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发表时间：
2008
影响因子：
3.6
通讯作者：
S. F. Martin
中科院分区：
文献类型：
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作者：
C. Lass;M. Vocanson;S. Wagner;C. Schempp;J. Nicolas;I. Merfort;S. F. Martin
翻译后摘要：倍半萜内酯（SL），从山金车的花头的次生植物代谢产物，发挥抗炎作用，主要是通过防止核因子（NF）-κB激活，因为烷基化的p65亚基。 尽管山金车具有已知的免疫抑制作用，但它已被归类为具有强烈诱导过敏性接触性皮炎的效力的植物。在这里，我们研究了SL作为抗炎化合物和接触性过敏原在体外和体内的双重作用。我们在小鼠接触性超敏反应模型中测试了SL的抗炎和致敏潜力。我们还使用树突状细胞来研究在不同剂量的SL存在下，体外NF-κB的活化和白细胞介素（IL）-12的分泌。山金车酊和SL在高浓度下有效抑制树突状细胞中NF-κB活化和IL-12产生，但在低浓度下具有免疫刺激作用。在小鼠模型中不能诱导接触性超敏反应，即使将山金车酊或SL未稀释地应用于发炎的皮肤。与此相反，山金车酊抑制接触过敏性强的接触致敏剂三硝基氯苯和树突状细胞的激活。然而，在急性CD 4缺失的MHC II基因敲除小鼠中，可诱导对山金车酊的接触性超敏反应。这些结果表明，山金车对接触性超敏反应的诱导可通过其抗炎作用和免疫抑制作用来预防，这是免疫活性小鼠免疫调节的结果。
Abstract: Sesquiterpene lactones (SL), secondary plant metabolites from flowerheads of Arnica, exert anti‐inflammatory effects mainly by preventing nuclear factor (NF)‐κB activation because of alkylation of the p65 subunit. Despite its known immunosuppressive action, Arnica has been classified as a plant with strong potency to induce allergic contact dermatitis. Here we examined the dual role of SL as anti‐inflammatory compounds and contact allergens in vitro and in vivo. We tested the anti‐inflammatory and allergenic potential of SL in the mouse contact hypersensitivity model. We also used dendritic cells to study the activation of NF‐κB and the secretion of interleukin (IL)‐12 in the presence of different doses of SL in vitro. Arnica tinctures and SL potently suppressed NF‐κB activation and IL‐12 production in dendritic cells at high concentrations, but had immunostimulatory effects at low concentrations. Contact hypersensitivity could not be induced in the mouse model, even when Arnica tinctures or SL were applied undiluted to inflamed skin. In contrast, Arnica tinctures suppressed contact hypersensitivity to the strong contact sensitizer trinitrochlorobenzene and activation of dendritic cells. However, contact hypersensitivity to Arnica tincture could be induced in acutely CD4‐depleted MHC II knockout mice. These results suggest that induction of contact hypersensitivity by Arnica is prevented by its anti‐inflammatory effect and immunosuppression as a result of immune regulation in immunocompetent mice.