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Subchronic exposure to concentrated ambient PM2.5 perturbs gut and lung microbiota as well as metabolic profiles in mice.
Environ Pollut. 2021 Mar 01; 272:115987.EP

Abstract

Exposure to ambient fine particular matter (PM2.5) are linked to an increased risk of metabolic disorders, leading to enhanced rate of many diseases, such as inflammatory bowel disease (IBD), cardiovascular diseases, and pulmonary diseases; nevertheless, the underlying mechanisms remain poorly understood. In this study, BALB/c mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CPM) for 2 months using a versatile aerosol concentration enrichment system(VACES). We found subchronic CPM exposure caused significant lung and intestinal damage, as well as systemic inflammatory reactions. In addition, serum and BALFs (bronchoalveolar lavage fluids) metabolites involved in many metabolic pathways in the CPM exposed mice were markedly disrupted upon PM2.5 exposure. Five metabolites (glutamate, glutamine, formate, pyruvate and lactate) with excellent discriminatory power (AUC = 1, p < 0.001) were identified to predict PM2.5 exposure related toxicities. Furthermore, subchronic exposure to CPM not only significantly decreased the richness and composition of the gut microbiota, but also the lung microbiota. Strong associations were found between several gut and lung bacterial flora changes and systemic metabolic abnormalities. Our study showed exposure to ambient PM2.5 not only caused dysbiosis in the gut and lung, but also significant systemic and local metabolic alterations. Alterations in gut and lung microbiota were strongly correlated with metabolic abnormalities. Our study suggests potential roles of gut and lung microbiota in PM2.5 caused metabolic disorders.

Authors+Show Affiliations

Department of Research, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, 1500 Zhouyuan Road, 201318, Shanghai, China; Inspection and Quarantine Department, The College of Medical Technology, Shanghai University of Medicine & Health Sciences, 279 Zhouzhu Road, 201318, Shanghai, China.State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Metabonomics and Systems Biology Laboratory at Shanghai International Centre for Molecular Phenomics, Fudan University, Shanghai, 200438, China.Department of Atmospheric and Oceanic Sciences & Institute of Atmospheric Sciences, Fudan University, Shanghai, China.Key Laboratory of Birth Defects and Reproductive Health of National Health and Family Planning Commission (Chongqing Key Laboratory of Birth Defects and Reproductive Health, Chongqing Population and Family Planning, Science and Technology Research Institute), Chongqing, 400020, China; State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.Department of Microbiology and Microbial Engineering, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, China.State Key Laboratory of Genetic Engineering, School of Life Sciences and Human Phenome Institute, Fudan University, Shanghai, China.Department of Oral & Maxillofacial - Head & Neck Oncology, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, 639 Zhi Zao Ju Road, Shanghai, 200011, China.Department of Oral & Maxillofacial - Head & Neck Oncology, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, 639 Zhi Zao Ju Road, Shanghai, 200011, China.State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China; Key Laboratory of Birth Defects and Reproductive Health of National Health and Family Planning Commission (Chongqing Key Laboratory of Birth Defects and Reproductive Health, Chongqing Population and Family Planning, Science and Technology Research Institute), Chongqing, 400020, China.Department of Microbiology and Microbial Engineering, School of Life Sciences, Fudan University, 2005 Songhu Road, Shanghai, 200438, China.The Core Laboratory in Medical Center of Clinical Research, Department of Molecular Diagnostic & Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University (SJTU) School of Medicine, Shanghai, 200011, China.Department of Oral & Maxillofacial - Head & Neck Oncology, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, 639 Zhi Zao Ju Road, Shanghai, 200011, China.The Core Laboratory in Medical Center of Clinical Research, Department of Molecular Diagnostic & Endocrinology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University (SJTU) School of Medicine, Shanghai, 200011, China. Electronic address: rui_li2020@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

33213950

Citation

Ran, Zihan, et al. "Subchronic Exposure to Concentrated Ambient PM2.5 Perturbs Gut and Lung Microbiota as Well as Metabolic Profiles in Mice." Environmental Pollution (Barking, Essex : 1987), vol. 272, 2021, p. 115987.
Ran Z, An Y, Zhou J, et al. Subchronic exposure to concentrated ambient PM2.5 perturbs gut and lung microbiota as well as metabolic profiles in mice. Environ Pollut. 2021;272:115987.
Ran, Z., An, Y., Zhou, J., Yang, J., Zhang, Y., Yang, J., Wang, L., Li, X., Lu, D., Zhong, J., Song, H., Qin, X., & Li, R. (2021). Subchronic exposure to concentrated ambient PM2.5 perturbs gut and lung microbiota as well as metabolic profiles in mice. Environmental Pollution (Barking, Essex : 1987), 272, 115987. https://doi.org/10.1016/j.envpol.2020.115987
Ran Z, et al. Subchronic Exposure to Concentrated Ambient PM2.5 Perturbs Gut and Lung Microbiota as Well as Metabolic Profiles in Mice. Environ Pollut. 2021 Mar 1;272:115987. PubMed PMID: 33213950.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Subchronic exposure to concentrated ambient PM2.5 perturbs gut and lung microbiota as well as metabolic profiles in mice. AU - Ran,Zihan, AU - An,Yanpeng, AU - Zhou,Ji, AU - Yang,Jingmin, AU - Zhang,Youyi, AU - Yang,Jingcheng, AU - Wang,Lei, AU - Li,Xin, AU - Lu,Daru, AU - Zhong,Jiang, AU - Song,Huaidong, AU - Qin,Xingjun, AU - Li,Rui, Y1 - 2020/11/03/ PY - 2020/07/17/received PY - 2020/10/12/revised PY - 2020/11/01/accepted PY - 2020/11/21/pubmed PY - 2021/2/11/medline PY - 2020/11/20/entrez KW - Inflammation KW - Metabonomics KW - Microtiota KW - PM2.5 SP - 115987 EP - 115987 JF - Environmental pollution (Barking, Essex : 1987) JO - Environ Pollut VL - 272 N2 - Exposure to ambient fine particular matter (PM2.5) are linked to an increased risk of metabolic disorders, leading to enhanced rate of many diseases, such as inflammatory bowel disease (IBD), cardiovascular diseases, and pulmonary diseases; nevertheless, the underlying mechanisms remain poorly understood. In this study, BALB/c mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CPM) for 2 months using a versatile aerosol concentration enrichment system(VACES). We found subchronic CPM exposure caused significant lung and intestinal damage, as well as systemic inflammatory reactions. In addition, serum and BALFs (bronchoalveolar lavage fluids) metabolites involved in many metabolic pathways in the CPM exposed mice were markedly disrupted upon PM2.5 exposure. Five metabolites (glutamate, glutamine, formate, pyruvate and lactate) with excellent discriminatory power (AUC = 1, p < 0.001) were identified to predict PM2.5 exposure related toxicities. Furthermore, subchronic exposure to CPM not only significantly decreased the richness and composition of the gut microbiota, but also the lung microbiota. Strong associations were found between several gut and lung bacterial flora changes and systemic metabolic abnormalities. Our study showed exposure to ambient PM2.5 not only caused dysbiosis in the gut and lung, but also significant systemic and local metabolic alterations. Alterations in gut and lung microbiota were strongly correlated with metabolic abnormalities. Our study suggests potential roles of gut and lung microbiota in PM2.5 caused metabolic disorders. SN - 1873-6424 UR - https://www.unboundmedicine.com/medline/citation/33213950/Subchronic_exposure_to_concentrated_ambient_PM2_5_perturbs_gut_and_lung_microbiota_as_well_as_metabolic_profiles_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0269-7491(20)36676-8 DB - PRIME DP - Unbound Medicine ER -