Traffic generated emissions alter the lung microbiota by promoting the expansion of Proteobacteria in C57Bl/6 mice placed on a high-fat diet.

Affiliation

Daniel S(1), Pusadkar V(2), McDonald J(3), Mirpuri J(4), Azad RK(5), Goven A(1), Lund AK(6).
Author information:
(1)Advanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX 76201, USA.
(2)BioDiscovery Institute, Department of Biological Sciences, University of North Texas, Denton, TX 76203, USA.
(3)Lovelace Biomedical and Environmental Research Institute, Albuquerque, NM 87108, USA.
(4)Division of Neonatal-Perinatal Medicine, Department of Pediatrics, UT Southwestern Medical Center, Dallas, TX 75390, USA.
(5)BioDiscovery Institute, Department of Biological Sciences, University of North Texas, Denton, TX 76203, USA; Department of Mathematics, University of North Texas, Denton, TX 76203, USA.
(6)Advanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX 76201, USA. Electronic address: [Email]

Abstract

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.