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首页> 外文期刊>The Journal of Experomental Medicine >Development of Eosinophilic Airway Inflammation and Airway Hyperresponsiveness in Mast Cell–deficient Mice
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Development of Eosinophilic Airway Inflammation and Airway Hyperresponsiveness in Mast Cell–deficient Mice

机译:肥大细胞缺乏小鼠嗜酸性气道炎症和气道高反应性的发展。

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Mast cells are the main effector cells of immediate hypersensitivity and anaphylaxis. Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence. To address these issues, mast cell–deficient mice ( W / W v ) and their congenic littermates were sensitized to ovalbumin (OVA) by intraperitoneal injection and subsequently challenged with OVA via the airways. Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice. Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar. These data indicate that mast cells or IgE–mast cell activation is not required for the development of eosinophilic inflammation and AHR in mice sensitized to allergen via the intraperitoneal route and challenged via the airways.
机译:肥大细胞是立即超敏和过敏反应的主要效应细胞。它们在变应原诱导的气道高反应性(AHR)发展中的作用是有争议的,并且基于间接证据。为了解决这些问题,通过腹膜内注射使肥大细胞缺陷小鼠(W / W v)及其同基因同窝小鼠对卵白蛋白(OVA)敏感,随后通过气道对其进行攻击。血清中OVA特异性免疫球蛋白E(IgE)水平和支气管肺泡灌洗液或肺部消化液中嗜酸性粒细胞数量的比较表明,两组小鼠之间没有差异。此外,在基线和吸入乙酰甲胆碱后气道阻力和动态顺应性的测量结果相似。这些数据表明,通过腹膜内途径对过敏原敏感并经气道攻击的小鼠,嗜酸性粒细胞炎症和AHR的发展不需要肥大细胞或IgE-肥大细胞活化。

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