Falcon-Rodriguez Carlos Iván, De Vizcaya-Ruiz Andrea, Rosas-Pérez Irma Aurora, Osornio-Vargas Álvaro Román, Segura-Medina Patricia
Posgrado en Ciencias Biológicas, Universidad Nacional Autónoma de México (UNAM), Av. Universidad 3000, Ciudad Universitaria (CU), Del. Coyoacán, C.P. 04510 Ciudad de México (CDMX), Mexico; Departamento de Investigación en Hiperactividad Bronquial, Instituto Nacional de Enfermedades Respiratorias (INER), Calz. de Tlalpan 4502, Col. Belisario Domínguez, Sección XVI, Del. Tlalpan, C.P. 14080 Ciudad de México (CDMX), Mexico.
Laboratorio de Toxicología de Contaminantes Atmosféricos y Estrés Oxidativo, Departamento de Toxicología, Centro de Investigaciones y Estudios Avanzados (CINVESTAV)-Zacatenco, Instituto Politécnico Nacional (IPN), Av. Instituto Politécnico Nacional 2508, Col. San Pedro Zacatenco, Del. Gustavo A. Madero, C.P. 07360 Ciudad de México (CDMX), Mexico.
Environ Pollut. 2017 Sep;228:474-483. doi: 10.1016/j.envpol.2017.05.050. Epub 2017 May 29.
Exposure to Particulate Matter (PM) could function as an adjuvant depending on the city of origin in mice allergic asthma models. Therefore, our aim was to determine whether inhalation of fine particles (PM2.5) from Mexico City could act as an adjuvant inducing allergic sensitization and/or worsening the asthmatic response in guinea pig, as a suitable model of human asthma. Experimental groups were Non-Sensitized (NS group), sensitized with Ovalbumin (OVA) plus Aluminum hydroxide (Al(OH)3) as adjuvant (S + Adj group), and sensitized (OVA) without adjuvant (S group). All the animals were exposed to Filtered Air (FA) or concentrated PM2.5 (5 h/daily/3 days), employing an aerosol concentrator system, PM2.5 composition was characterized. Lung function was evaluated by barometric plethysmography (Penh index). Inflammatory cells present in bronchoalveolar lavage were counted as well as OVA-specific IgG1 and IgE were determined by ELISA assay. Our results showed in sensitized animals without Al(OH)3, that the PM2.5 exposure (609 ± 12.73 μg/m3) acted as an adjuvant, triggering OVA-specific IgG1 and IgE concentration. Penh index increased ∼9-fold after OVA challenge in adjuvant-sensitized animals as well as in S + PM2.5 group (∼6-fold), meanwhile NS + FA and S + FA lacked response. S + Adj + PM2.5 group showed an increase significantly of eosinophils and neutrophils in bronchoalveolar lavage. PM2.5 composition was made up of inorganic elements and Polycyclic Aromatic Hydrocarbons, as well as endotoxins and β-glucan, all these components could act as adjuvant. Our study demonstrated that acute inhalation of PM2.5 acted as an adjuvant, similar to the aluminum hydroxide effect, triggering allergic asthma in a guinea pig model. Furthermore, in sensitized animals with aluminum hydroxide an enhancing influence of PM2.5 exposure was observed as specific-hyperresponsiveness to OVA challenge (quickly response) and eosinophilic and neutrophilic airway inflammation. Fine particles from Mexico City is a complex mix, which play a significant role as adjuvant in allergic asthma.
在小鼠过敏性哮喘模型中，根据颗粒物（PM）的来源城市不同，其可能起到佐剂的作用。因此，我们的目的是确定吸入来自墨西哥城的细颗粒物（PM2.5）是否能作为一种佐剂，在豚鼠（一种适合人类哮喘的模型）中诱导过敏性致敏和/或加重哮喘反应。实验分组为未致敏组（NS组）、用卵清蛋白（OVA）加氢氧化铝（Al(OH)3）作为佐剂致敏组（S + 佐剂组）和不用佐剂的致敏组（S组）。所有动物均暴露于过滤空气（FA）或浓缩的PM2.5（每天5小时/共3天），使用气溶胶浓缩系统，对PM2.5的成分进行了表征。通过气压体积描记法（Penh指数）评估肺功能。对支气管肺泡灌洗中的炎性细胞进行计数，并通过酶联免疫吸附测定法（ELISA）测定OVA特异性IgG1和IgE。我们的结果表明，在没有Al(OH)3的致敏动物中，PM2.5暴露（609 ± 12.73 μg/m3）起到了佐剂的作用，引发了OVA特异性IgG1和IgE浓度升高。在佐剂致敏动物以及S + PM2.5组中，OVA激发后Penh指数增加了约9倍（S + PM2.5组约为6倍），而NS + FA组和S + FA组则无反应。S + 佐剂 + PM2.5组支气管肺泡灌洗中的嗜酸性粒细胞和中性粒细胞显著增加。PM2.5的成分由无机元素、多环芳烃以及内毒素和β-葡聚糖组成，所有这些成分都可能起到佐剂的作用。我们的研究表明，急性吸入PM2.5起到了佐剂的作用，类似于氢氧化铝的作用，在豚鼠模型中引发过敏性哮喘。此外，在使用氢氧化铝致敏的动物中，观察到PM2.5暴露对OVA激发的特异性高反应性（快速反应）以及嗜酸性粒细胞和中性粒细胞气道炎症有增强作用。来自墨西哥城的细颗粒物是一种复杂的混合物，在过敏性哮喘中作为佐剂发挥着重要作用。
