探究颗粒物对小鼠屋尘螨和卵清蛋白过敏性气道炎症的影响。
Investigating the Effects of Particulate Matter on House Dust Mite and Ovalbumin Allergic Airway Inflammation in Mice.
作者信息
Castañeda Alejandro R, Pinkerton Kent E
机构信息
Center for Health and the Environment, University of California, Davis, California.
Department of Pediatrics, School of Medicine, University of California, Davis, California.
出版信息
Curr Protoc Toxicol. 2016 May 4;68:18.18.1-18.18.18. doi: 10.1002/cptx.5.
Particulate matter (PM), a component of air pollution, has been shown to enhance allergen-mediated airway hypersensitivity and inflammation. Surprisingly, exposure to PM during the sensitization to allergen is sufficient to produce immunological changes that result in heightened inflammatory effects upon future allergen exposures (challenge) in the absence of PM. This suggests that PM has the ability to modulate the allergic immune response, thereby acting as an adjuvant by enhancing the immunological memory formed during the adaptive immune response; however, the mechanisms through which this occurs remain elusive. Establishing a reproducible animal model to study the PM-mediated immunotoxicological effects that enhance allergy, may provide insights to understand how air pollution activates the immune system and thereby modulates the pathophysiology of asthma. The basic protocol can be used to study various characteristics of air pollution, such as PM size, source, or chemical composition, to help elucidate how such features may affect the allergic response in a mouse model of asthma. Using a BALB/c model of acute exposure (14 days), mice are first sensitized with allergen and PM, and then subsequently challenged with allergen only. The endpoints of this basic protocol include the assessment of inflammation via cells recovered from broncho-alveolar lavage (BAL), histopathological analysis, gene expression profiles, and protein quantification of inflammatory markers. © 2016 by John Wiley & Sons, Inc.
颗粒物(PM)是空气污染的一个组成部分,已被证明会增强变应原介导的气道高反应性和炎症。令人惊讶的是,在对变应原致敏期间暴露于PM足以产生免疫变化,从而在未来不存在PM的情况下再次接触变应原(激发)时导致更强的炎症效应。这表明PM有能力调节过敏性免疫反应,从而通过增强适应性免疫反应期间形成的免疫记忆而起到佐剂的作用;然而,其发生的机制仍然不清楚。建立一个可重复的动物模型来研究PM介导的增强过敏的免疫毒理学效应,可能有助于深入了解空气污染如何激活免疫系统,进而调节哮喘的病理生理学。该基本方案可用于研究空气污染的各种特征,如PM大小、来源或化学成分,以帮助阐明这些特征如何在哮喘小鼠模型中影响过敏反应。使用急性暴露(14天)的BALB/c模型,小鼠首先用变应原和PM致敏,然后仅用变应原进行激发。该基本方案的终点包括通过支气管肺泡灌洗(BAL)回收的细胞评估炎症、组织病理学分析、基因表达谱以及炎症标志物的蛋白质定量。© 2016约翰威立国际出版公司