Far from the Eyes, Close to the Heart: Dysbiosis of Gut Microbiota and Cardiovascular Consequences

Sérino, Matteo; Blasco-Baqué, Vincent; Simón, Nicolás; Burcelin, Rémy

doi:10.1007/s11886-014-0540-1

Cited by 88 publications

(68 citation statements)

References 59 publications

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“…Nevertheless, contrasting results can be found in the literature with regard to the metabolic impact of microbial-generated metabolites from phosphatidylcholine, such as trimethylamine (TMA) and TMA-N-oxide (TMAO) [49]. In detail, regarding the human enterotype classification [50], the enterotype Prevotella is associated with higher blood levels of TMAO than the enterotype Bacteroides in humans [51].…”

Section: Cardiac Mirsmentioning

confidence: 99%

MicroRNAs: Decoders of Dysbiosis into Metabolic Diseases?

Sérino¹

2016

J Diabetes Metab

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The identification of molecular factors bridging gut microbiota dysbiosis to alterations of host metabolism still remains a major goal in biomedical research. In fact, on one hand, there is a worldwide consensus about the systemic impact, from brain to liver, from heart to adipose tissue, of gut microbiota dysbiosis. On the other hand, beyond the microbial production of short chain fatty acids and their vast metabolic properties, little is known about the molecular mechanisms linking a change in the activity of gut microbes to a modification of host cell metabolism. In this context, microRNAs (also known as miRs) are promising molecules which could allow explaining how dysbiosis is converted into metabolic outcomes since: 1-miRs are pleiotropic regulators of gene expression, targeting multiple mRNAs at once; 2-miRs expression in specific organs such as the intestine has been demonstrated to be under the control of gut microbiota; 3-alterations in miRs expression have been found in the majority of tissues targeted by gut microbiota dysbiosis during metabolic diseases such as liver, adipose tissue, pancreas, skeletal muscle, intestine, heart and also the brain. In this review publications in the growing field of miRsbased metabolic control at a systemic level will be discussed together with a putative link with gut microbiota dysbiosis.

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Section: Cardiac Mirsmentioning

confidence: 99%

MicroRNAs: Decoders of Dysbiosis into Metabolic Diseases?

Sérino¹

2016

J Diabetes Metab

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“…Recently, alterations in gut microbiota composition and metabolic potential have been identified as contributing factors in CVD development (46,61). In particular, trimethylamine N-oxide (TMAO), the hepatic oxidation product of the colon microbial metabolite TMA, has gained a lot of attention as a potential promoter of atherosclerosis (49).…”

Section: Trimethylamine: a Microbial Metabolite Contributing To Athermentioning

confidence: 99%

Microbiology Meets Big Data: The Case of Gut Microbiota–Derived Trimethylamine

Falony¹,

Vieira-Silva²,

Raes

2015

Annu. Rev. Microbiol.

140

105

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During the past decade, meta-omics approaches have revolutionized microbiology, allowing for a cultivation-free assessment of the composition and functional properties of entire microbial ecosystems. On the one hand, a phylogenetic and functional interpretation of such data relies on accumulated genetic, biochemical, metabolic, and phenotypic characterization of microbial variation. On the other hand, the increasing availability of extensive microbiome data sets and corresponding metadata provides a vast, underused resource for the microbiology field as a whole. To demonstrate the potential for integrating big data into a functional microbiology workflow, we review literature on trimethylamine (TMA), a microbiota-generated metabolite linked to atherosclerosis development. Translating recently elucidated microbial pathways resulting in TMA production into genomic orthologs, we demonstrate how to mine for their presence in public (meta-) genomic databases and link findings to associated metadata. Reviewing pathway abundance in public data sets shows that TMA production potential is associated with symptomatic atherosclerosis and allows identification of currently uncharacterized TMA-producing bacteria.

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“…Dysregulation of the gut microbiome has been implicated in a number of diseases (Moore and Moore 1995;Ley et al 2005;Turnbaugh et al 2006;Bollyky et al 2009;Damman et al 2012;Serino et al 2014), and is associated with environmental stimuli such as diet (Penders et al 2005;Turnbaugh et al 2009), stress (Bailey, Lubach and Coe 2004), antibiotics (Tanaka et al 2009), infection (Barman et al 2008) and environmental contaminants such as subtherapeutic antimicrobials (Cho et al 2012) and xeno-biotics (Zhang et al 2015). Typically, bacterial dysbiosis is either a direct response to therapeutics (e.g.…”

Section: Introductionmentioning

confidence: 99%

TCDD influences reservoir of antibiotic resistance genes in murine gut microbiome

Stedtfeld¹,

Stedtfeld²,

Fader

et al. 2017

FEMS Microbiology Ecology

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One sentence summary: An environmental toxicant that is not a metal, biocide or antimicrobial indirectly (via a non-inflammatory host response) influences the reservoir of antibiotic resistance genes in the murine gut. Editor: Kornelia Smalla ABSTRACTDysbiosis of the gut microbiome via antibiotics, changes in diet and infection can select for bacterial groups that more frequently harbor antimicrobial resistance genes (ARGs) and mobile genetic elements (MGEs). However, the impact of environmental toxicants on the reservoir of ARGs in the gut microbiome has received less attention. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent aryl hydrocarbon receptor (AhR) agonist with multiple toxic health effects including immune dysfunction. The selective pressure of TCDD on the abundance of ARG and MGE-harboring gut populations was examined using C57BL/6 mice exposed to 0-30 μg/kg TCDD for 28 and 92 days with the latter having a 30-day recovery period. DNA extracted from temporally collected fecal pellets was characterized using a qPCR array with 384 assays targeting ARGs and MGEs. Fourteen genes, typically observed in Enterobacteriaceae, increased significantly within 8 days of initial dosing, persisted throughout the treatment period, and remained induced 30 days post dosing. A qPCR primer set targeting Enterobacteriaceae also showed 10-to 100-fold higher abundance in TCDD-treated groups, which was further verified using metagenomics. Results show a bloom of ARG-harboring bacterial groups in the gut due to a xenobiotic compound that is not a metal, biocide or antimicrobial.

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Far from the Eyes, Close to the Heart: Dysbiosis of Gut Microbiota and Cardiovascular Consequences

Cited by 88 publications

References 59 publications

MicroRNAs: Decoders of Dysbiosis into Metabolic Diseases?

MicroRNAs: Decoders of Dysbiosis into Metabolic Diseases?

Microbiology Meets Big Data: The Case of Gut Microbiota–Derived Trimethylamine

TCDD influences reservoir of antibiotic resistance genes in murine gut microbiome

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