Alejandro R. Castañeda, Kent E. Pinkerton
{"title":"Investigating the Effects of Particulate Matter on House Dust Mite and Ovalbumin Allergic Airway Inflammation in Mice","authors":"Alejandro R. Castañeda, Kent E. Pinkerton","doi":"10.1002/cptx.5","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":72743,"journal":{"name":"Current protocols in toxicology","volume":"68 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2016-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/cptx.5","citationCount":"15","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current protocols in toxicology","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cptx.5","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 15
Abstract
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.
颗粒物质对小鼠屋尘螨和卵清蛋白过敏性气道炎症的影响
颗粒物(PM)是空气污染的一个组成部分,已被证明会增强过敏原介导的气道过敏和炎症。令人惊讶的是,在过敏原致敏过程中暴露于PM足以产生免疫学变化,导致在没有PM的情况下,在未来的过敏原暴露(挑战)中炎症效应加剧。这表明PM具有调节过敏性免疫反应的能力,从而通过增强适应性免疫反应中形成的免疫记忆而起到佐剂的作用;然而,这种情况发生的机制仍然难以捉摸。建立一个可重复的动物模型来研究pm介导的免疫毒理学效应,从而增强过敏,可能为了解空气污染如何激活免疫系统从而调节哮喘的病理生理提供见解。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影响哮喘小鼠模型的过敏反应。采用急性暴露(14天)BALB/c模型,首先用过敏原和PM致敏小鼠,然后仅用过敏原致敏小鼠。该基本方案的终点包括通过支气管肺泡灌洗(BAL)恢复的细胞来评估炎症、组织病理学分析、基因表达谱和炎症标志物的蛋白质定量。©2016 by John Wiley &儿子,Inc。
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