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Establishment of airway eosinophilic bronchitis mouse model without hyperresponsiveness by ovalbumin

机译:卵清蛋白无高反应性的气道嗜酸性支气管炎小鼠模型的建立

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Eosinophilic bronchitis (EB) is a useful tool for studying airway hyperresponsiveness (AHR), but an exact EB animal model is lacking. Our objective was to establish an EB mouse model using ovalbumin (OVA). Mice were divided into asthma, normal saline (NS) control and three model groups. Asthma mice were challenged intranasally with 200 μg OVA. Model groups were challenged with one of the three OVA doses (10, 20 or 100 μg), and NS control mice received normal saline. Changes in lung resistance (RL), serum OVA-specific immunoglobulin-E (IgE) and differential inflammatory cell counts in bronchoalveolar lavage fluid (BALF) were determined after exposure to increasing doses of methacholine (MCh). Lung histological sections were examined for inflammatory infiltration. RL in the 10-μg OVA-challenged model group was not significantly different compared with the NS group at any MCh concentration but was significantly different compared with the asthma group (P < 0.01). RL in the other two model groups was intermediate between the asthma and NS groups. Serum OVA-specific IgE and eosinophils in BALF were increased significantly in all model and asthma groups compared with the NS group, but no significant differences were observed between model and asthma groups. Inflammatory cells were seen around bronchioles and capillaries in model and asthma groups but not the NS group. A mouse model of EB without AHR can be established by 10 μg OVA challenge and provides a useful tool for studying AHR mechanisms.
机译:嗜酸性支气管炎(EB)是研究气道高反应性(AHR)的有用工具,但缺乏确切的EB动物模型。我们的目标是使用卵清蛋白(OVA)建立EB小鼠模型。将小鼠分为哮喘,生理盐水(NS)对照和三个模型组。用200μgOVA鼻内攻击哮喘小鼠。用三种OVA剂量(10、20或100μg)之一挑战模型组,NS对照小鼠接受生理盐水。暴露于增加剂量的乙酰甲胆碱(MCh)后,测定肺阻力(R L ),血清OVA特异性免疫球蛋白-E(IgE)和支气管肺泡灌洗液(BALF)中不同的炎症细胞计数的变化。 。检查肺组织切片的炎性浸润。在任何MCh浓度下,10μgOVA挑战模型组的R L 与NS组相比无显着差异,但与哮喘组相比有显着差异(P <0.01)。另外两个模型组的R L 介于哮喘和NS组之间。与NS组相比,所有模型组和哮喘组中BALF中的血清OVA特异性IgE和嗜酸性粒细胞均显着增加,但模型组和哮喘组之间未观察到显着差异。模型组和哮喘组的细支气管和毛细血管周围可见炎性细胞,而NS组则没有。不含AHR的EB小鼠模型可以通过10μgOVA挑战建立,并为研究AHR机制提供了有用的工具。

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