Human gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA290897 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2128100.fastq.gz | Fastqsanger.gz | |||
| SRR2128110.fastq.gz | Fastqsanger.gz | |||
| SRR2128120.fastq.gz | Fastqsanger.gz | |||
| SRR2128130.fastq.gz | Fastqsanger.gz | |||
| SRR2128140.fastq.gz | Fastqsanger.gz |
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Project description:Human microbiota profile after 35-day beta-glucan intervention
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Project description:Background & Aims: Non-alcoholic fatty liver disease (NALFLD)-associated changes in gut microbiota are important drivers of disease progression toward fibrosis. Therefore, reversing microbiota alterations could ameliorate NAFLD progression. Oat beta-glucan, a non-digestible polysaccharides, has shown promising therapeutic effects on hyperlipidemia associated with NAFLD, but its impact on gut microbiota and most importantly NAFLD fibrosis remains unknown. Methods: We performed detailed metabolic phenotyping including body composition, glucose tolerance, and lipid metabolism as well as comprehensive characterization of the gut-liver axis in a western-style diet (WSD)-induced model of NAFLD and assessed the effect of a beta-glucan intervention on early and advanced liver disease. Gut microbiota was modulated using broad-spectrum antibiotic (Abx) treatment. Results: Oat beta-glucan supplementation did not affect WSD-induced body weight gain, glucose intolerance, and the metabolic phenotype remained largely unaffected. Interestingly, oat beta-glucan dampened NAFLD inflammation, associated with significantly reduced monocyte-derived macrophages (MoMFs) infiltration, fibroinflammatory gene expression, and strongly reduced fibrosis development. Mechanistically, this protective effect was not mediated by changes in bile acid composition or signaling, but was dependent on gut microbiota and was lost upon Abx treatment. Specifically, oat beta-glucan partially reversed unfavorable changes in gut microbiota, resulting in an expansion of protective taxa, including Ruminococcus, and Lactobacillus followed by reduced translocation of TLR ligands. Conclusions: Our findings identify oat beta-glucan as a highly efficacious food supplement that dampens inflammation and fibrosis development in diet-induced NAFLD. These results, along with its favorable dietary profile, suggest that it may be a cost-effective and well-tolerated approach to preventing NAFLD progression and should be assessed in clinical studies.
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Project description:We established a bacteria infective intestinal inflammation in turbot (Scophthalmus maximus). And found that β-glucan could significantly alleviate the phenotype of turbot intestinal inflammation. We performed single cell transcriptome analysis to study bacteria infective intestinal inflammation and the effects of β-glucan. Furthermore, we revealed that β-glucan through activates Th17 cells to alleviate intestinal inflammation in turbot.
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Project description:To evaluate the DC genome-wide gene expression in response to beta-glucan and its regulation by IL-1 receptor antagonist (IL-1RA) we used a whole genome microarray. The gene expression profiling was performed in DC left untreated or exposed to beta-glucan for 4 and 12 h, in absence or presence of IL-1RA. This strategy allowed the identification of early/immediate and late/secondary genes regulated by beta-glucan in an IL-1-dependent and -independent manner. Human monocyte-derived DC were obtained by a 6/7-d cultures of freshly isolated monocytes with recombinant human IL-4 (10 ng/ml) and GM-CSF (50 ng/ml). Beta-glucan-associated gene expression and its regulation by IL-1RA in human DC was measured in cells left untreated or at 4 and 12 h after exposure to 10 ug/ml of particulate beta-glucan in absence or presence of 2.5 ug/ml of IL-1RA. Five different conditions (Untreated 0h, beta-glucan 4h, IL-1RA + beta-glucan 4h, beta-glucan 12h, and IL-1RA + beta-glucan 12h) were tested using DC from three different donors.
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Project description:Human intestinal microbiota Raw sequence reads
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Project description:A clone encoding carboxymethylcellulase activity was isolated during functional screening of a human gut metagenomic library using Lactococcus lactis MG1363 as heterologous host. The insert sequence revealed a glycoside hydrolase family 9 (GH9) catalytic domain with sequence similarity to a gene from Coprococcus sp. ART55/1, which is closely related to Coprocococcus eutactus. Surveys of available genomes indicated a limited distribution of GH9 domains among dominant human colonic anaerobes. Genomes of two Coprococcus-related strains showed the presence of two GH9-encoding and four GH5-encoding genes, however, the strains did not appear to be able to degrade cellulose. Instead, they grew well on beta-glucans and one of the strains also showed growth on galactomannan, galactan and glucomannan. Gene expression and proteomic analysis of Coprococcus sp. ART55/1 grown on cellobiose, beta-glucan and lichenan led to a similar change in expression in comparison to glucose. On beta-glucan and lichenan only, one of the four GH5 genes was strongly upregulated. Growth on glucomannan lead to a transcriptional response of many genes, in particular a strong upregulation of glycoside hydrolases involved in mannan degradation. Thus, beta-glucans are a major growth substrate for species related to Coprococcus eutactus, with glucomannan and galactans alternative substrates for some strains.
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Project description:The gut bacterium Coprococcus sp. ART55/1 has been found to encode two genes containing glycoside hydrolase family 9 (GH9) catalytic domains. These genes are hypothesised to impact upon the ability of this bacteria to utilise different carbon sources. To further investigate the role of these genes, as well as the wider transcriptome, Coprococcus sp. ART55/1 was grown on five different carbon sources - beta-glucan, lichenan, cellobiose, glucose and glucomannan - and the transcriptional response was investigated using RNA sequencing.
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