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Surfactant protein D inhibits early airway response in Aspergillus fumigatus-sensitized mice.

机译:表面活性剂蛋白D抑制烟曲霉敏感小鼠的早期气道反应。

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The surfactant protein SP-D has been reported to reduce bronchial hyper-responsiveness, blood eosinophilia, and T-helper type 2 cytokines in models of allergic asthma. However, little is known about the functional effect of SP-D on the early airway response upon allergen inhalation, which is an important feature of this disease. We investigated whether SP-D is able to reduce the immediate allergen-induced mediator release and the early bronchial obstruction in addition to its effects on airway inflammation and bronchial hyperresponsiveness in an Aspergillus fumigatus mouse asthma model. A. fumigatus-sensitized mice were treated with a recombinant fragment of human SP-D or placebo. Lung functions were measured in orotracheally intubated, spontaneously breathing animals using body plethysmography. In addition, passively sensitized precision-cut lung slices (PCLS) were used to determine the effect of SP-D on allergen-induced histamine release. SP-D inhibited the allergen-induced early airway response and reduced airway hyperresponsiveness compared with placebo. Eosinophilia in bronchoalveolar lavage and lung tissue was reduced after SP-D treatment, possibly by reducing eotaxin levels in the lung. Furthermore, SP-D treatment reduced the allergen-induced histamine release from PCLS. These data suggest that SP-D not only reduces allergen-induced eosinophilic inflammation and airway hyperresponsiveness but also provides protection against early airway obstruction by inhibition of early mediator release.
机译:据报道,在过敏性哮喘模型中,表面活性剂蛋白SP-D可降低支气管高反应性,血液嗜酸性粒细胞增多和2型T辅助细胞因子。然而,关于SP-D对过敏原吸入后早期气道反应的功能影响知之甚少,这是该疾病的重要特征。我们研究了SP-D在烟曲霉小鼠哮喘模型中,除了对气道炎症和支气管高反应性的影响外,是否还能够减少过敏原诱导的介质释放和早期支气管阻塞。用人SP-D或安慰剂的重组片段治疗烟曲霉致敏的小鼠。使用人体体积描记法测量口气管插管,自发呼吸的动物的肺功能。此外,使用被动敏化的精密切割肺切片(PCLS)来确定SP-D对变应原诱导的组胺释放的影响。与安慰剂相比,SP-D抑制了变应原诱导的早期气道反应,并降低了气道高反应性。 SP-D处理后,支气管肺泡灌洗液和肺组织中的嗜酸性粒细胞减少,可能是通过降低肺中的趋化因子水平。此外,SP-D处理减少了过敏原诱导的组胺从PCLS释放。这些数据表明,SP-D不仅可以减少变应原诱导的嗜酸性粒细胞炎症和气道高反应性,而且还可以通过抑制早期介质释放来提供针对早期气道阻塞的保护作用。

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