Advanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX 76201, USA.
BioDiscovery Institute, Department of Biological Sciences, University of North Texas, Denton, TX 76203, USA.
Ecotoxicol Environ Saf. 2021 Apr 15;213:112035. doi: 10.1016/j.ecoenv.2021.112035. Epub 2021 Feb 11.
Air pollution has been documented to contribute to severe respiratory diseases like asthma and chronic obstructive pulmonary disorder (COPD). Although these diseases demonstrate a shift in the lung microbiota towards Proteobacteria, the effects of traffic generated emissions on lung microbiota profiles have not been well-characterized. Thus, we investigated the hypothesis that exposure to traffic-generated emissions can alter lung microbiota and immune defenses. Since a large population of the Western world consumes a diet rich in fats, we sought to investigate the synergistic effects of mixed vehicle emissions and high-fat diet consumption. We exposed 3-month-old male C57Bl/6 mice placed either on regular chow (LF) or a high-fat (HF: 45% kcal fat) diet to mixed emissions (ME: 30 µg PM/m gasoline engine emissions+70 µg PM/m diesel engine emissions) or filtered air (FA) for 6 h/d, 7 d/wk for 30 days. Levels of pulmonary immunoglobulins IgA, IgG, and IgM were analyzed by ELISA, and lung microbial profiling was done using qPCR and Illumina 16 S sequencing. We observed a significant decrease in lung IgA in the ME-exposed animals, compared to the FA-exposed animals, both fed a HF diet. Our results also revealed a significant decrease in lung IgG in the ME-exposed animals both on the LF diet and HF diet, in comparison to the FA-exposed animals. We also observed an expansion of Enterobacteriaceae belonging to the Proteobacteria phylum in the ME-exposed groups on the HF diet. Collectively, we show that the combined effects of ME and HF diet result in decreased immune surveillance and lung bacterial dysbiosis, which is of significance in lung diseases.
空气污染已被证实会导致严重的呼吸系统疾病，如哮喘和慢性阻塞性肺疾病（COPD）。尽管这些疾病显示肺部微生物组向变形菌门（Proteobacteria）转移，但交通产生的排放物对肺部微生物组谱的影响尚未得到很好的描述。因此，我们假设暴露于交通产生的排放物会改变肺部微生物组和免疫防御。由于西方世界的很大一部分人口食用富含脂肪的饮食，我们试图研究混合车辆排放物和高脂肪饮食摄入的协同作用。我们将 3 个月大的雄性 C57Bl/6 小鼠暴露于混合排放物（ME：30µg PM/每克汽油发动机排放物+70µg PM/每克柴油发动机排放物）或过滤空气（FA）中，每天 6 小时，每周 7 天，持续 30 天。通过 ELISA 分析肺免疫球蛋白 IgA、IgG 和 IgM 的水平，并通过 qPCR 和 Illumina 16S 测序进行肺部微生物组分析。我们观察到，与暴露于 FA 的 HF 饮食喂养的动物相比，ME 暴露的动物的肺部 IgA 水平显著降低。我们的结果还表明，与暴露于 FA 的动物相比，无论是 LF 饮食还是 HF 饮食，ME 暴露的动物的肺部 IgG 水平均显著降低。我们还观察到在 HF 饮食的 ME 暴露组中，变形菌门（Proteobacteria）的肠杆菌科（Enterobacteriaceae）的数量显著增加。总之，我们表明 ME 和 HF 饮食的综合作用导致免疫监视减少和肺部细菌失调，这在肺部疾病中具有重要意义。
