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小鼠哮喘的“经典”卵清蛋白激发模型。

The "classical" ovalbumin challenge model of asthma in mice.

作者信息

Kumar Rakesh K, Herbert Cristan, Foster Paul S

机构信息

Department of Pathology, School of Medical Sciences, University of New South Wales, Sydney, Australia.

出版信息

Curr Drug Targets. 2008 Jun;9(6):485-94. doi: 10.2174/138945008784533561.

DOI:10.2174/138945008784533561
PMID:18537587
Abstract

Ovalbumin challenge models of asthma offer many opportunities for increasing our understanding of the pathogenetic mechanisms underlying this disease, as well as for identifying novel therapeutic targets. There is no single "classical" model, because numerous alternatives exist with respect to the choice of mouse strain, method of sensitisation, route and duration of challenge, and approach to assessing the host response. Moreover, the limitations of these models need to be recognised when attempting to interpret experimental findings. Nevertheless, careful use of well-defined models allows investigators to answer specific questions that are otherwise difficult to address.

摘要

哮喘的卵清蛋白激发模型为增进我们对该疾病发病机制的理解以及识别新的治疗靶点提供了诸多机会。不存在单一的“经典”模型,因为在小鼠品系的选择、致敏方法、激发途径和持续时间以及评估宿主反应的方法等方面存在众多替代方案。此外,在试图解释实验结果时,需要认识到这些模型的局限性。然而,谨慎使用定义明确的模型可使研究人员回答那些否则难以解决的特定问题。

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[Again an asthma model... but a useful one].[又是一个哮喘模型……但却是个有用的模型]
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Suppression of asthma-like responses in different mouse strains by oral tolerance.口服耐受对不同小鼠品系哮喘样反应的抑制作用。
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Establishing the phenotype in novel acute and chronic murine models of allergic asthma.在新型急性和慢性过敏性哮喘小鼠模型中确定表型。
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Modeling airway remodeling: the winner by a nose?气道重塑建模:仅以微弱优势获胜?
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Mast cell involvement in the adenosine mediated airway hyper-reactivity in a murine model of ovalbumin-induced lung inflammation.在卵清蛋白诱导的肺部炎症小鼠模型中,肥大细胞参与腺苷介导的气道高反应性。
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