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Pulmonary eosinophilia correlates with allergen deposition to the lower respiratory tract in a mouse model of asthma.

机译:肺嗜酸性粒细胞症与哮喘小鼠模型中的下呼吸道的过敏原沉积相关。

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BACKGROUND: Eosinophilic infiltration into the airways is frequently associated with allergic asthma; however, the role of antigen deposition in mediating this phenomenon has not been studied in detail. OBJECTIVE: Using a murine model of ovalbumin (OVA) allergy, we examined how differential deposition of OVA during antigen challenge affects pulmonary eosinophilia, immune response and airway hyper-reactivity (AHR). METHODS: Differential allergen deposition to the upper respiratory tract (URT) alone or combined upper and lower respiratory tract (ULRT) was accomplished by administering OVA intranasally to either anaesthetized or unanaesthetized mice, respectively. BALB/c mice (6-7 weeks old) were sensitized with OVA-alum via the intraperitoneal route, and then challenged intranasally using OVA, with or without anaesthesia. AHR, enumeration of inflammatory cells and quantitative measurement of inflammatory cytokines and chemokines in bronchoalveolar lavage fluid (BALF), lung histopathology and immune responses were subsequently assessed. RESULTS: In sensitized animals challenged via the ULRT route, a profound eosinophilia and goblet cell hyperplasia was observed in lung tissue. Conversely, sensitized mice receiving an identical challenge dose via the URT route alone exhibited only negligible levels of inflammation. Interestingly, AHR and OVA-specific IgG(1) and IgE systemic responses were comparable between the two groups. CONCLUSION: This study indicates that direct exposure of allergen in the deep lung is highly correlated with airway eosinophilia and lung inflammation, but does not correlate with AHR or immune response.
机译:背景:嗜酸性渗透到气道中经常与过敏性哮喘有关;然而,抗原沉积在介导这种现象中的作用尚未详细研究。目的:使用卵烧蛋白(OVA)过敏的鼠模型,我们研究了抗原攻击期间OVA的差异沉积如何影响肺嗜酸性粒细胞,免疫应答和气道超反应性(AHR)。方法:通过鼻内鼻内施用OVA至麻醉或未展开的小鼠,通过将卵巢施用卵巢或未展开的小鼠来完成单独或组合的上呼吸道(URT)对上呼吸道(URT)的差分过敏原。 Balb / c小鼠(6-7周龄)通过腹膜内途径与OVA-Alum敏感,然后使用ova,有或没有麻醉攻击鼻内攻击。随后评估AHR,炎症细胞的诱发细胞和炎性细胞因子和趋化因子的定量测量,肺组织病理学和免疫应答。结果:在通过ULRT途径挑战的敏化动物中,在肺组织中观察到深度嗜酸性粒细胞和脚酚细胞增生。相反,通过单独的URT途径接受相同挑战剂量的敏化小鼠仅表现出可忽略的炎症水平。有趣的是,AHR和OVA特异性IgG(1)和IgE全身反应在两组之间可相当。结论:本研究表明,深肺过敏原直接暴露与气道嗜酸性粒细胞和肺炎高度相关,但与AHR或免疫应答无关。

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