期刊论文详细信息
Particle and Fibre Toxicology
Diesel exhaust particles alter the profile and function of the gut microbiota upon subchronic oral administration in mice
Adrien Paquot1  Giulio G. Muccioli1  Jérôme Ambroise2  Caroline Bouzin3  Margaux Rappe4  Dominique Lison4  Sybille van den Brule4  Chantal Dessy5 
[1] Bioanalysis and Pharmacology of Bioactive Lipids Research Group, Louvain Drug Research Institute, UCLouvain, Brussels, Belgium;Centre de Technologies Moléculaires Appliquées, Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium;IREC Imaging Platform (2IP), Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium;Louvain centre for Toxicology and Applied Pharmacology, Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium;Pole of Pharmacology and Therapeutics, Institut de Recherche Expérimentale et Clinique, UCLouvain and Cliniques Universitaires Saint-Luc, Brussels, Belgium;
关键词: Air pollution;    Particles;    Cardiovascular diseases;    Metabolic diseases;    Short-chain fatty acids;    Atherosclerosis;    ApoE;   
DOI  :  10.1186/s12989-021-00400-7
来源: Springer
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【 摘 要 】

BackgroundAmbient air pollution by particulate matters, including diesel exhaust particles (DEP), is a major cause of cardiovascular and metabolic mortality worldwide. The mechanisms by which DEP cause these adverse outcomes are not completely understood. Because the gut microbiota controls cardiovascular and metabolic health, we hypothesized that the fraction of inhaled DEP which reach the gut after mucociliary clearance and swallowing might induce gut dysbiosis and, in turn, contribute to aggravate or induce cardiovascular and metabolic diseases.ResultsFemale ApoE−/− mice fed a Western diet, and wild-type (C57Bl/6) mice fed standard diet were gavaged with DEP (SRM2975) doses corresponding to mucociliary clearance from inhalation exposure (200 or 1000 ng/day, 3 times a week for 3 months; and 40, 200 or 1000 ng/day, 3 times a week for 6 months, respectively). No mortality, overt systemic or digestive toxicity was observed. A dose-dependent alteration of the gut microbiota was recorded in both strains. In ApoE−/−, β-diversity was modified by DEP, but no significant modification of the relative abundance of the phyla, families or genera was identified. In C57BL/6 mice, DEP reduced α-diversity (Shannon and Simpson indices), and modified β-diversity, including a reduction of the Proteobacteria and Patescibacteria phyla, and an increase of the Campylobacterota phylum. In both mouse models, perturbation of the gut microbiota composition was associated with a dose-dependent reduction of bacterial short chain fatty acids (butyrate and propionate) in cecal content. However, DEP ingestion did not aggravate (ApoE−/−), or induce (C57BL/6 mice) atherosclerotic plaques, and no metabolic alteration (glucose tolerance, resistance to insulin, or lipidemia) was recorded.ConclusionsWe show here that oral exposure to DEP, at doses relevant for human health, changes the composition and function of the gut microbiota. These modifications were, however, not translated into ultimate atherosclerotic or metabolic outcomes.

【 授权许可】

CC BY   

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