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Traffic generated emissions alter the lung microbiota by promoting the expansion of Proteobacteria in C57Bl/6 mice placed on a high-fat diet
Ecotoxicology and Environmental Safety ( IF 6.8 ) Pub Date : 2021-02-11 , DOI: 10.1016/j.ecoenv.2021.112035
Sarah Daniel , Vaidehi Pusadkar , Jacob McDonald , Julie Mirpuri , Rajeev K. Azad , Art Goven , Amie K. Lund

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/m3 gasoline engine emissions + 70 µg PM/m3 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.



中文翻译:

交通产生的排放物通过促进高脂饮食的C57Bl / 6小鼠中变形杆菌的扩增来改变肺微生物群。

空气污染已被证明可导致严重的呼吸系统疾病,例如哮喘和慢性阻塞性肺疾病(COPD)。尽管这些疾病显示出肺微生物群向Proteobacteria的转变,但是交通产生的排放物对肺微生物群特征的影响尚未得到很好的表征。因此,我们研究了以下假设:交通产生的排放物暴露会改变肺部微生物群和免疫防御能力。由于西方世界的大量人口食用富含脂肪的饮食,因此我们试图研究混合排放车辆和高脂饮食的协同作用。我们将3个月大的雄性C57Bl / 6小鼠暴露于普通食物(LF)或高脂(HF:45%大卡脂肪)饮食中,混合排放(ME:30 µg PM / m 3汽油发动机排放量 +  70 µg PM / m 3柴油机排放)或过滤后的空气(FA)进行6天/天,7天/周的30天。通过ELISA分析肺免疫球蛋白IgA,IgG和IgM的水平,并使用qPCR和Illumina 16 S测序进行肺微生物谱分析。我们观察到,与暴露于FA的动物相比,暴露于ME的动物均饲喂HF日粮,其肺IgA显着降低。我们的研究结果还表明,与暴露于FA的动物相比,接受LF和HF饮食的ME暴露动物的肺IgG显着降低。我们还观察到在HF饮食中,暴露于ME的人群中属于门氏杆菌的肠杆菌科细菌的扩增。总体而言,我们表明,ME和HF饮食的联合作用导致免疫监测降低和肺细菌营养不良,这在肺部疾病中具有重要意义。

更新日期:2021-02-11
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