Ontology highlight
ABSTRACT:
PROVIDER: PRJNA666083 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12727500.fastq.gz | Fastqsanger.gz | |||
| SRR12727501.fastq.gz | Fastqsanger.gz | |||
| SRR12727502.fastq.gz | Fastqsanger.gz | |||
| SRR12727503.fastq.gz | Fastqsanger.gz | |||
| SRR12727504.fastq.gz | Fastqsanger.gz |
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Project description:The microorganisms colonizing the gastrointestinal tract of animals, collectively referred to as the gut microbiome, affect numerous host behaviors dependent on the central nervous system (CNS). Studies comparing germ-free mice to normally colonized mice have demonstrated influences of the microbiome on anxiety-related behaviors, voluntary activity, and gene expression in the CNS. Additionally, there is epidemiologic evidence supporting an intergenerational influence of the maternal microbiome on neurodevelopment of offspring and behavior later in life. There is limited experimental evidence however directly linking the maternal microbiome to long-term neurodevelopmental outcomes, or knowledge regarding mechanisms responsible for such effects. Here we show that that the maternal microbiome has a dominant influence on several offspring phenotypes including anxiety-related behavior, voluntary activity, and body weight. Adverse outcomes in offspring were associated with features of the maternal microbiome including bile salt hydrolase (Bsh) expression, abundance of certain bile acids, and hepatic expression of S1pr2. In cross-foster experiments, offspring resembled their birth dam phenotypically, despite faithful colonization in the postnatal period with the surrogate dam microbiome. Genome-wide methylation analysis of hippocampal DNA identified microbiome-associated differences in methylation of 196 loci in total, 176 of which were imprinted by the maternal microbiome. Further, single-cell transcriptional analysis revealed accompanying differences in expression of several differentially methylated genes within certain hippocampal cell clusters, and vascular expression of genes associated with bile acid transport. Inferred cell-to-cell communication in the hippocampus based on coordinated ligand-receptor expression revealed differences in expression of neuropeptides associated with satiety. Collectively, these data provide proof-of-principle that the maternal gut microbiome has a dominant influence on the neurodevelopment underlying certain offspring behaviors and activities, and selectively affects genome methylation and gene expression in the offspring CNS in conjunction with that neurodevelopment.
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Project description:HuMiChip was used to analyze human oral and gut microbiomes, showing significantly different functional gene profiles between oral and gut microbiome. The results were used to demonstarte the usefulness of applying HuMiChip to human microbiome studies.
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Project description:The Vaginal Microbiome, Maternal Response, and Preterm Birth
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Project description:The Vaginal Microbiome, Maternal Response, and Preterm Birth
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Project description:Feed additives aiming to improve gastrointestinal health are frequently supplied to piglets after weaning but might be more effective when administered before weaning. In this period, feed additives can either be administered directly to neonates, or indirectly via sow’s feed. It is yet unknown what the effect of the administration route is on gut functionality and health. Therefore, we compared the effect of different dietary interventions on gut functionality after maternal administration (lactation feed) to the neonatal administration route (oral gavage). These feed interventions included medium chain fatty acids (MCFA), beta-glucans (BG), and galacto-oligosaccharides (GOS). We measured intestinal gene expression and microbiota composition after birth (d1) and after weaning (d31). Our results show that the type of intervention and the administration route influence gut functionality (microbiome and gene expression profiles). MCFA administration led to a more differentially orchestrated response when comparing the neonatal and maternal administration route then the other two additives, indicating the route of administration of the feed interventions is determinative for the outcome. This implies that for each nutritional intervention in early life of a pig the optimal route of administration needs to be determined.
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Project description:<p>This is a study of the oral and gut microbiome of 226 mother-child dyads enrolled in the INSIGHT (Intervention Nurses Start Infants Growing on Healthy Trajectories) study. INSIGHT is a randomized, controlled trial comparing a responsive parenting intervention designed for the primary prevention of childhood obesity against a control. </p> <p>The microbiome portion of the study was designed to investigate the relationship between a cross-sectional view of the child's microbiome (at two years of age) and the patterns of growth between birth and 2 years. These first-born children were deeply studied in this time period with data collected on a wide variety of variables including mode of delivery, sex, weight and height (collected at 7 time points), medication usage, diet information, and maternal health information (gestational weight gain, gestational diabetes, smoking during pregnancy). Microbiome samples from the child (buccal swab and stool sample) and their mother (buccal swab) were collected at the child's 2-year clinical research visit. </p>
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Project description:“Dysbiosis" of the maternal gut microbiome, in response to environmental challenges such as infection, altered diet and stress during pregnancy, has been increasingly associated with abnormalities in offspring brain function and behavior. However, whether the maternal gut microbiome regulates neurodevelopment in the absence of environmental challenge remains unclear. In addition, whether the maternal microbiome exerts such influences during critical periods of embryonic brain development is poorly understood. Here we investigate how depletion, and selective reconstitution, of the maternal gut microbiome influences fetal neurodevelopment in mice. Embryos from antibiotic-treated and germ-free dams exhibit widespread transcriptomic alterations in the fetal brain relative to conventionally-colonized controls, with reduced expression of several genes involved in axonogenesis. In addition, embryos from microbiome-depleted mothers exhibit deficient thalamocortical axons and impaired thalamic axon outgrowth in response to cell-extrinsic guidance cues and growth factors. Consistent with the importance of fetal thalamocortical axonogenesis for shaping neural circuits for sensory processing, restricted depletion of the maternal microbiome from pre-conception through mid-gestation yields offspring that exhibit tactile hyposensitivity in select sensorimotor behavioral tasks. Gnotobiotic colonization of antibiotic-treated dams with a limited consortium of spore-forming bacteria indigenous to the gut microbiome prevents abnormalities in fetal brain gene expression, fetal thalamocortical axonogenesis and adult tactile sensory behavior associated with maternal microbiome depletion. Metabolomic profiling reveals that the maternal microbiota regulates levels of numerous small molecules in the maternal serum as well as the brains of fetal offspring. Select microbiota-dependent metabolites – trimethylamine N-oxide, 5-aminovalerate, imidazole propionate, and hippurate – sufficiently promote axon outgrowth from fetal thalamic explants. Moreover, maternal supplementation with the metabolites during early gestation abrogates deficiencies in fetal thalamocortical axons and prevents abnormalities in tactile sensory behavior in offspring from microbiome-depleted dams. Altogether, these findings reveal that the maternal gut microbiome promotes fetal thalamocortical axonogenesis and select tactile sensory behaviors in mice, likely by signaling of microbially modulated metabolites to neurons in the developing brain.
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