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首页> 外文期刊>Clinical and experimental allergy : >Interference of methysergide, a specific 5-hydroxytryptamine receptor antagonist, with airway chronic allergic inflammation and remodelling in a murine model of asthma.
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Interference of methysergide, a specific 5-hydroxytryptamine receptor antagonist, with airway chronic allergic inflammation and remodelling in a murine model of asthma.

机译：甲基异麦角酰胺（一种特定的5-羟色胺受体拮抗剂）对哮喘小鼠模型的气道慢性过敏性炎症和重塑的干扰。

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BACKGROUND: Airway remodelling encompasses the structural changes observed in asthmatic airways. Mast cells, through the release of histamine and 5-hydroxytryptamine (serotonin), are implicated in early asthmatic reactions, bronchoconstriction and mucosal oedema, and in the development of bronchial hyperresponsiveness. However, the association between serotonin and remodelling processes in murine model of airways inflammation remains to be elucidated. OBJECTIVE: As serotonin is released by murine mast cells upon antigen challenge, we tested the hypothesis of its involvement in the development of inflammatory and remodelling processes in a murine model of chronic airway inflammation following prolonged allergen challenge. Methods BALB/c mice were exposed to aerosolized ovalbumin for 20 min 2 days a week, for 4 consecutive weeks. Two hours before each challenge, they were treated with methysergide (intranasally, 40 microg/kg). Forty-eight hours after the last aerosol challenge, bronchoalveolar lavage (BAL) and lung tissue were collected for analysis. RESULTS: Methysergide inhibited the allergen-induced increase in airway eosinophilia, reduced T helper type 2 (Th2) cytokines in lung, spleen or thoracic lymph nodes, and specific IgE levels. The extravasation of plasma and fibronectin production in the lung, and collagen deposition in the lung were also inhibited after methysergide treatment. Although methysergide treatment induced an increase in IFN-gamma levels, experiments with neutralizing antibody suggest that this is not responsible for inhibition. In addition, instillation of serotonin to immunized mice induced eosinophil recruitment to BAL, Th2 cytokine production and fibronectin release in lung as well as collagen deposition. CONCLUSION: Serotonin may contribute to the development and maintenance of remodelling through the release of cytokines and of fibrogenic mediators. Serotonin should therefore be considered as relevant for the development and maintenance of airway remodelling.
机译：背景：气道重塑包括在哮喘气道中观察到的结构变化。肥大细胞通过释放组胺和5-羟色胺（5-羟色胺）而参与早期哮喘反应，支气管收缩和粘膜水肿以及支气管高反应性的发展。然而，在气道炎症的鼠模型中5-羟色胺与重塑过程之间的关联仍有待阐明。目的：由于血清抗原在受到抗原攻击后由鼠肥大细胞释放，因此我们在长期变应原攻击后的慢性气道炎症鼠模型中测试了其参与炎症和重塑过程发展的假说。方法将BALB / c小鼠每周2天暴露于雾化的卵清蛋白20分钟，连续4周。每次攻击前两个小时，均用美塞麦特（鼻内40微克/千克）治疗。在最后一次气雾剂攻击后的48小时内，收集了支气管肺泡灌洗液（BAL）和肺组织进行分析。结果：美塞麦肽抑制变应原诱导的气道嗜酸性粒细胞增多，肺，脾或胸淋巴结中的T辅助2型（Th2）细胞因子减少以及特定的IgE水平。甲基异麦角酰胺治疗后，肺中血浆和纤连蛋白生成的外渗以及肺中胶原蛋白的沉积也受到抑制。尽管甲基化麦角肽治疗诱导了IFN-γ水平的增加，但中和抗体的实验表明这与抑制作用无关。此外，向免疫小鼠滴注5-羟色胺会诱导嗜酸性粒细胞募集到BAL，Th2细胞因子的产生和肺中纤连蛋白的释放以及胶原蛋白的沉积。结论：5-羟色胺可能通过释放细胞因子和纤维化介质来促进重塑的发展和维持。因此，应将5-羟色胺与发展和维持气道重塑有关。

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