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首页> 外文期刊>Clinical and experimental allergy : >Local administration of uridine suppresses the cardinal features of asthmatic airway inflammation.
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Local administration of uridine suppresses the cardinal features of asthmatic airway inflammation.

机译：尿苷的局部给药抑制哮喘气道炎症的基本特征。

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BACKGROUND: The immuno-modulatory properties of nucleotides such as adenosine or inosine, have been described extensively. Recently, the nucleoside uridine and its analogue 4-thiouridine have gained attention for their protective role in acute lung inflammation. OBJECTIVE: In this study, we investigated the influence of uridine on asthmatic airway inflammation. METHODS: We used the classical ovalbumin (OVA)-alum model, as well as a model of house dust mite-(HDM)-induced airway inflammation. The degree of inflammation was determined by bronchoalveolar lavage (BAL), histology, and measurement of bronchial hyperresponsiveness. RESULTS: Intratracheal treatment of OVA-sensitized animals with uridine before allergen challenge resulted in a reduction in total BAL cells and BAL eosinophils. This was accompanied by reduced tissue infiltration and diminished production of T helper type 2-cytokines by mediastinal lymph node cells. Additionally, mice treated with uridine developed less bronchial hyperresponsiveness. Uridine was also effective in reducing airway inflammation in HDM-induced asthma. The protective effects of uridine were independent of myeloid dendritic cell (mDC) function, because in vitro pre-treatment of allergen-pulsed DCs with uridine did not alter the degree of inflammation. However, uridine inhibited the release of pro-inflammatory mediators in vivo and by cultured lung epithelial cells, suggesting an effect on lung structural cells. CONCLUSION: In summary, we were able to show that uridine inhibits the classical features of asthmatic airway inflammation. As uridine supplementation is well tolerated in humans, it might be a new therapeutic approach for the treatment of bronchial asthma.
机译：背景：已经广泛地描述了诸如腺苷或肌苷等核苷酸的免疫调节特性。最近，核苷尿苷及其类似物4-硫尿苷因其在急性肺部炎症中的保护作用而受到关注。目的：本研究调查了尿苷对哮喘气道炎症的影响。方法：我们使用了经典的卵清蛋白（OVA）-alum模型，以及屋尘螨（HDM）诱导的气道炎症模型。炎症程度通过支气管肺泡灌洗（BAL），组织学和支气管高反应性测定来确定。结果：在变应原攻击前用尿苷对OVA致敏动物进行气管内治疗导致总BAL细胞和BAL嗜酸性粒细胞减少。这伴随着纵隔淋巴结细胞的组织浸润减少和T辅助2型细胞因子的产生减少。另外，用尿苷处理的小鼠出现较少的支气管高反应性。尿苷还可以有效减少HDM诱发的哮喘中的气道炎症。尿苷的保护作用与髓样树突细胞（mDC）功能无关，因为在体外用尿苷预处理变应原刺激的DC不会改变炎症程度。然而，尿苷在体内和培养的肺上皮细胞中抑制促炎性介质的释放，表明对肺结构细胞的作用。结论：总的来说，我们能够证明尿苷抑制哮喘气道炎症的经典特征。由于尿苷补充剂在人类中耐受良好，因此它可能是治疗支气管哮喘的新治疗方法。

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