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首页> 外文期刊>Inhalation toxicology >Exposure of adult mice to environmental tobacco smoke fails to enhance the immune response to inhaled antigen.
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Exposure of adult mice to environmental tobacco smoke fails to enhance the immune response to inhaled antigen.

机译：成年小鼠暴露于环境烟草烟雾中无法增强对吸入抗原的免疫反应。

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Epidemiologic evidence supports a role for environmental tobacco smoke (ETS) in the occurrence and severity of allergies/asthma. However, neither the precise combination of ETS and allergen exposure nor the mechanism (or mechanisms) by which these factors interact and contribute to asthma induction is known. Animal model studies have failed to establish a convincing relationship between ETS exposure and asthma induction, perhaps because of methodological inadequacies. Here, we tested the hypothesis that ETS inhalation would provoke an asthmatic response by overcoming normal airway tolerance to inhaled antigens. Our protocol combined daily ETS exposure with nose-only sensitization to ovalbumin. Three strains of mice were tested, each with a different level of susceptibility to airway hypersensitivity. Immunological responses were assessed by immunoglobulin production. Airway inflammation was assessed by bronchoalveolar lavage differentials and lung histopathology. Airway hyperresponsiveness was determined by methacholine challenge. The mice produced ovalbumin-specific antibodies following ovalbumin exposure in a strain-dependent manner. Only the A/J mice produced detectable levels of ovalbumin-specific immunoglobulin (Ig) E. Both A/J and BALB/c mice produced ovalbumin-specific IgG1 antibodies. The C57Bl/6 mice did not produce detectable levels of antibodies. The A/J mice also exhibited airway inflammation following ovalbumin exposure. Neither the C57Bl/6 nor the BALB/c mice exhibited signs of airway inflammation. Exposure to ETS failed to enhance ovalbumin-specific antibody production, airway inflammation, or hyperresponsiveness. Together these results indicate that ETS exposure accompanied by nose-only allergen sensitization fails to overcome aerosol tolerance in adult mice.
机译：流行病学证据支持环境烟草烟雾（ETS）在过敏/哮喘的发生和严重程度中的作用。然而，既不知道ETS和过敏原暴露的精确组合，也不知道这些因素相互作用并促成哮喘的机制。动物模型研究未能在ETS暴露与哮喘诱导之间建立令人信服的关系，这可能是由于方法学上的不足。在这里，我们测试了以下假设：ETS吸入将克服正常的呼吸道对吸入抗原的耐受性，从而引发哮喘反应。我们的方案将每日ETS暴露与仅鼻子对卵白蛋白的致敏相结合。测试了三种小鼠，每种小鼠对气道超敏反应的敏感性不同。通过免疫球蛋白的产生来评估免疫反应。通过支气管肺泡灌洗液差异和肺组织病理学评估气道炎症。气道高反应性由乙酰甲胆碱激发确定。在卵白蛋白暴露后，小鼠以应变依赖性方式产生卵白蛋白特异性抗体。仅A / J小鼠产生可检测水平的卵白蛋白特异性免疫球蛋白（Ig）E。A/ J和BALB / c小鼠均产生卵白蛋白特异性IgG1抗体。 C57Bl / 6小鼠未产生可检测水平的抗体。卵清蛋白暴露后，A / J小鼠也表现出气道炎症。 C57Bl / 6和BALB / c小鼠均未表现出气道炎症迹象。暴露于ETS不能增强卵白蛋白特异性抗体的产生，气道炎症或反应过度。这些结果共同表明，ETS暴露并伴有仅鼻过敏原致敏不能克服成年小鼠的气溶胶耐受性。

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