Seymour Brian W P, Schelegle Edward S, Pinkerton Kent E, Friebertshauser Kathleen E, Peake Janice L, Kurup Viswanath P, Coffman Robert L, Gershwin Laurel J
Department of Pathology, Microbiology and Immunology, 1126 Haring Hall, School of Veterinary Medicine, University of California, One Shields Avenue, Davis, CA 95616, USA.
Clin Dev Immunol. 2003 Mar;10(1):35-42. doi: 10.1080/10446670310001598483.
Involuntary inhalation of tobacco smoke has been shown to aggravate the allergic response. Antibodies to fungal antigens such as Aspergillus fumigatus (Af) cause an allergic lung disease in humans. This study was carried out to determine the effect of environmental tobacco smoke (ETS) on a murine model of allergic bronchopulmonary aspergillosis (ABPA). BALB/c mice were exposed to aged and diluted sidestream cigarette smoke to simulate 'second-hand smoke'. The concentration was consistent with that achieved in enclosed public areas or households where multiple people smoke. During exposure, mice were sensitized to Af antigen intranasally. Mice that were sensitized to Af antigen and exposed to ETS developed significantly greater airway hyperreactivity than did mice similarly sensitized to Af but housed in ambient air. The effective concentration of aerosolized acetylcholine needed to double pulmonary flow resistance was significantly lower in Af + ETS mice compared to the Af + AIR mice. Immunological data that supports this exacerbation of airway hyperresponsiveness being mediated by an enhanced type 1 hypersensitivity response include: eosinophilia in peripheral blood and lung sections. All Af sensitized mice produced elevated levels of IL4, IL5 and IL10 but no IFN-gamma indicating a polarized Th2 response. Thus, ETS can cause exacerbation of asthma in ABPA as demonstrated by functional airway hyperresponsiveness and elevated levels of blood eosinophilia.
已证明非自愿吸入烟草烟雾会加重过敏反应。针对烟曲霉（Af）等真菌抗原的抗体可导致人类患过敏性肺病。本研究旨在确定环境烟草烟雾（ETS）对过敏性支气管肺曲霉病（ABPA）小鼠模型的影响。将BALB/c小鼠暴露于老化和稀释的侧流香烟烟雾中，以模拟“二手烟”。其浓度与在多人吸烟的封闭公共场所或家庭中达到的浓度一致。在暴露期间，通过鼻内给予使小鼠对Af抗原致敏。与同样对Af致敏但饲养在环境空气中的小鼠相比，对Af抗原致敏并暴露于ETS的小鼠出现了明显更高的气道高反应性。与Af + AIR组小鼠相比，Af + ETS组小鼠使肺血流阻力加倍所需的雾化乙酰胆碱有效浓度显著更低。支持这种气道高反应性加剧是由增强的1型超敏反应介导的免疫学数据包括：外周血和肺组织切片中的嗜酸性粒细胞增多。所有对Af致敏的小鼠IL4、IL5和IL10水平均升高，但未产生IFN-γ，表明存在极化的Th2反应。因此，如功能性气道高反应性和血液嗜酸性粒细胞水平升高所示，ETS可导致ABPA患者哮喘加重。
