Bifidobacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA351747 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5015150.fastq.gz | Fastqsanger.gz | |||
| SRR5015160.fastq.gz | Fastqsanger.gz | |||
| SRR5015180.fastq.gz | Fastqsanger.gz | |||
| SRR5015190.fastq.gz | Fastqsanger.gz | |||
| SRR5015260.fastq.gz | Fastqsanger.gz |
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Project description:Effects of dietary yogurt consumption on the gastrointestinal (GI) microbial communities of healthy human subjects
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Project description:With the aim of investigating the genome-wide postprandial effects of single servings ingestion of milk and yogurt on gene expression in the blood cells of human subjects and to identify the downstream physiological processes regulated by the differentially expressed genes we conducted a randomized, controlled, single blinded, crossover study on 6 healthy male individuals. 540g of milk or yogurt was ingested after an overnight fasting. Blood samples were collected before (0h) and 2h, 4h, 6h after the ingestion and the blood cell transcriptome was analyzed using a linear kinetic analysis.
2010-10-01 | E-MEXP-2571 | biostudies-arrayexpress
Project description:Meta-analyses suggest that yogurt consumption reduces type 2 diabetes incidence in humans, but the molecular basis of these observations remains unknown. Here we show that dietary yogurt intake preserves whole-body glucose homeostasis and prevents hepatic insulin resistance and liver steatosis in a dietary mouse model of obesity-linked type 2 diabetes. Fecal microbiota transplantation studies reveal that these effects are partly linked to the gut microbiota. We further show that yogurt intake impacts the hepatic metabolome, notably maintaining the levels of branched chain hydroxy acids (BCHA) which correlate with improved metabolic parameters. These metabolites are generated upon milk fermentation and concentrated in yogurt. Remarkably, diet-induced obesity reduces plasma and tissue BCHA levels, and this is partly prevented by dietary yogurt intake. We further show that BCHA improve insulin action on glucose metabolism in liver and muscle cells, identifying BCHA as cell-autonomous metabolic regulators and potential mediators of yogurt's health effects.
2022-02-03 | MTBLS442 | MetaboLights
Project description:We performed the long-term administration experiment using a yogurt fermented with Lactobacillus delbrueckii subsp. bulgaricus 2038 and Streptococcus thermophilus 1131 (LB81 yogurt) for 20 months in order to understand the effects of the long-term intake of probiotics on mice. Microarrays were used to compare the gene expressions of the intestine, liver and spleen tissues between control mice and LB81 yogurt-intake mice at 28 months of age. Abbreviations used: A, LB81 yogurt-intake mice; C, control mice
2018-06-02 | GSE104375 | GEO
Project description:Inflammatory bowel diseases encompass gastrointestinal illnesseses typified by chronic inflammation, loss of epithelial integrity and gastrointestinal microbiota dysbiosis. In an effort to counteract these characteristic perturbations, we used stem cells and/or a probiotic preparation in a murine model of Dextran Sodium Sulfate induced colitis to examine both their efficacy in ameliorating disease and impact on niche-specific microbial communities of the lower GI tract. Colitis was induced in C57BL/6 mice by administering 3% DSS in drinking water for 10 days prior to administering one of three treatment plans: daily probiotic (VSL#3) supplementation for 3 days, a single tail vein injection of 1x106 murine mesenchymal stem cells, or both. Controls included DSS-untreated mice and DSS-treated mice that received no therapy. Ileal, cecal and colonic sections were collected for microbiota and histological analyses. Microbiota profiling revealed distinct bacterial community compositions in the ileum, cecum and colon of control untreated animals, all of which were predicted in silico to be enriched for a number of discrete KEGG pathways, indicating compositional and functional niche specificity in healthy animals. DSS- treatment perturbed community composition in all three niches with ileal communities exhibiting the greatest change relative to control animals. Stem cell, VSL#3 and the combination treated animals exhibited treatment-specific microbiota composition in the lower GI tract, though disease scores were only improved in VSL#3 treated animals. This VSL#3-associated shift in the ileal microbiota was characterized by significant Enterobacteriaceae enrichment compared to colitic animals (p<0.05),
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Project description:The mucosa that lines the gastrointestinal (GI) tracts is an important portal of entry for pathogens and provides the frontline of immune defense against HIV infection. Epithelial barrier dysfunction during HIV infection has largely been attributed to the rapid and severe depletion of CD4 T cells in the gastrointestinal (GI) tract. In this study, the poential role of small non-coding microRNA (miRNA) to contribute to epithelial dysfunction was investigated in the non-human primate SIV model and microarrays were utilized to determine changes in mucosal gene expression (non-miRNA) that could be correlated to miRNA modulatiolns. Microarrays were used to characterize changes in gene expression in the jejunal mucosa that occur during chronic SIV infection Jejunum tissues from healthy uninfected macaques and macaques with chronic stage SIV infection were used for RNA extraction and hybridization on Affymetrix microarrays.
2014-02-27 | E-GEOD-55359 | biostudies-arrayexpress
Project description:The lesions of enamel caries can be considered as the outcome of dysbiotic changes in the biofilm community of supragingival dental plaque. Demineralization occurs as the cumulative outcome of repeated shifts towards a less diverse microbiota that produces and tolerates a low pH environment in tooth sites that are sheltered from protective factors in host saliva. Although the etiology of caries is multifactorial, frequent consumption of foods rich in fermentable carbohydrates, notably sucrose, appears to be one of the major factors driving the microbiota in the direction of dysbiosis, particularly in the case of otherwise healthy children with normal salivary flow. Streptococcus mutans and closely related species (such as Streptococcus sobrinus) have long been considered to play a primary etiological role in dental caries. S. mutans responds to sucrose by producing large quantities of lactic acid. It is very tolerant of low pH, and produces an insoluble extracellular polysaccharide that may sequester acid at tooth surfaces. The mechanisms behind those putative virulence factors have been intensively studied in monoculture, and recently in simple multi-species consortia. Much less is known of other species that may also contribute to or protect against dysbiosis driven by dietary carbohydrates. Some strains of “non-mutans” streptococci produce and tolerate acid at levels comparable to S. mutans, while others show increased ariginolytic capabilities, which may act to raise pH within the biofilm matrix. S. mutans tends to be a minority species even in caries-active children, and carious lesions likewise can occur in children with no detectable S. mutans. 16S rDNA-based metagenomic comparisons of caries-active and caries-free subjects have detected associations between caries and a variety of oral species, including not only non-mutans streptococci, but also members of other genera, such as Scardovia and Bifidobacterium. Caries associations have not been consistent between studies. Moreover, different taxonomic clusters have been defined as subgroups within the same study. This raises an important point. Although caries-associated communities are typically less diverse than healthy supragingival plaque overall, those dysbiotic communities still display considerable taxonomic diversity between affected individuals. That in turn raises the question of whether it is desirable to define biomarkers of dysbiosis that are less dependent on taxonomy. The Human Microbiome project generated comprehensive metagenomic data for a wide variety of body sites in healthy subjects, including supragingival plaque. Although most of that data was based on 16S rDNA sequencing, shotgun metagenomics was also used to catalog the functional potential of all microbial genes within a smaller subset of subjects. One of the key findings was that healthy sites from different people were broadly similar with respect to their functional profiles, even though there was extensive individual variation in their taxonomic profiles. It is possible that the “conservation of function” concept may also extend to dysbiotic communities. This would explain why microbial communities associated with caries still show considerable taxonomic variation. In that case, differential patterns of community-wide gene and/or protein expression might provide a more accurate indicator of dysbiosis than can be achieved by counting caries-associated species. Metatranscriptomic or metaproteomic approaches can be used to provide information on function. A recent metatranscriptomic comparison of subgingival plaque from healthy and periodontally diseased sites in three subjects has provided data that support the “conservation of function” concept. They observed that taxonomically diverse diseased sites shared conserved gene expression profiles [20]. By the same token, a recent metaproteomic comparison of gut microbiotas from healthy controls to Crohn’s disease patients found that major shifts in protein expression by function did not always correlate with changes in taxon relative abundance [21]. In this metaproteomic study, we found that sucrose–induced changes in protein expression patterns for pathways involving glycolysis, lactate production, aciduricity and ammonia/glutamate metabolism were likewise conserved in taxonomically diverse dysbiotic oral microcosm biofilm communities.
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