Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1114027 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29097800_1.fastq.gz | Fastqsanger.gz | |||
| SRR29097800_2.fastq.gz | Fastqsanger.gz | |||
| SRR29097801_1.fastq.gz | Fastqsanger.gz | |||
| SRR29097801_2.fastq.gz | Fastqsanger.gz | |||
| SRR29097802_1.fastq.gz | Fastqsanger.gz |
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Project description:Within the human gut reside diverse microbes coexisting with the host in a mutually advantageous relationship. We comprehensively identified the modulatory effects of phylogenetically diverse human gut microbes on the murine intestinal transcriptome. Gene-expression profiles were generated from the whole-tissue intestinal RNA of mice colonized with various single microbial strains. The selection of microbe-specific effects, from the transcriptional response, yielded only a small number of transcripts, indicating that symbiotic microbes have only limited effects on the gut transcriptome overall. Moreover, none of these microbe-specific transcripts was uniformly induced by all microbes. Interestingly, these responsive transcripts were induced by some microbes but repressed by others, suggesting different microbes can have diametrically opposed consequences.
2017-02-16 | GSE88919 | GEO
Project description:We report the application of bulk RNA-sequencing-based technology for high-throughput profiling to examine the individual and combinatorial effects of the liver circadian clock and gut microbes on the liver transcriptome over 24-hours. Principle Component Analysis demonstrated that functionality of the liver circadian clock is the primary driver of the hepatic transcriptome profile, and presence of microbes is the secondary driver. We identified a range of significantly oscillating transcripts within each experimental group using empirical_JTK_CYCLE, and revealed an overall increase in oscillating transcripts with both the loss of cuntional liver clock and gut microbes. Network analysis via Spearman correlation revealed that a broken liver clock results in increased connections and correlated transcripts only in the presence of gut microbes. Finally, we show by differential expression and gene set enrichment analysis that several key metabolic pathways, particularly carbohydrate and lipid metabolism, were significantly downregulated when the liver clock is broken, regardless of microbial status. This study demonstrates the complex contributions of the liver circadian clock and gut microbes in transcriptome programming, both over time and overall.
2022-06-06 | GSE184303 | GEO
Project description:Coronary artery disease (CAD) is a widespread heart condition caused by atherosclerosis and influences millions of people worldwide. Early detection of CAD is challenging due to the lack of specific biomarkers. The gut microbiota and host-microbiota interactions have been well documented to affect human health. However, investigation that reveals the role of gut microbes in CAD is still limited. This study aims to uncover the synergistic effects of host genes and gut microbes associated with CAD through integrative genomic analyses.
2023-10-15 | GSE242047 | GEO
Project description:Coronary artery disease (CAD) is a widespread heart condition caused by atherosclerosis and influences millions of people worldwide. Early detection of CAD is challenging due to the lack of specific biomarkers. The gut microbiota and host-microbiota interactions have been well documented to affect human health. However, investigation that reveals the role of gut microbes in CAD is still limited. This study aims to uncover the synergistic effects of host genes and gut microbes associated with CAD through integrative genomic analyses.
2023-10-15 | GSE242046 | GEO
Project description:Intestinal microorganisms impact on health maintaining gut homeostasis and shaping the host immunity, while gut dysbiosis associates with many conditions including autism, a complex neurodevelopmental disorder with multifactorial aetiology. In autism, gut dysbiosis correlates with symptom severity and is characterized by a reduced bacterial variability and a diminished beneficial commensal relationship. Microbiota can influence the expression of host microRNAs that, in turn, regulate the growth of intestinal bacteria by means of bidirectional host-gut micro-biota cross-talk. We investigated possible interactions among intestinal microbes and between them and host transcriptional modulators in autism. To this purpose, we analysed, by “omics” technologies, faecal microbiome, mycobiome and small non-coding-RNAs (particularly miRNAs and piRNAs) of children with autism and neurotypical development. Patients displayed gut dysbiosis, related to a reduction of healthy gut micro- and mycobiota, and up-regulated tran-scriptional modulators. The targets of dysregulated non-coding-RNAs are involved in intestinal permeability, inflammation and autism. Furthermore, microbial families, underrepresented in patients, participate to the production of human essential metabolites negatively influencing the health condition. Here, we propose a novel approach to analyse faeces as a whole and, for the first time, we detected miRNAs and piRNAs in faecal samples of patients with autism.
2022-03-12 | GSE198199 | GEO
Project description:Obesity is a risk factor for Osteoarthritis (OA), the greatest cause of disability in the US. The impact of obesity on OA is driven by systemic inflammation, now understood to be caused by an altered gut microbiome. Oligofructose, a non-digestible prebiotic fiber, can correct the obese gut microbiome, suggesting a novel approach to treat the OA of obesity. Here we report that in the obese murine gut, beneficial Bifidobacteria are lost while key proinflammatory species gain in abundance. A downstream systemic inflammatory signature culminates with accelerated knee OA. Oligofructose supplementation corrects the obese gut microbiome in part by supporting key commensal microflora, particularly Bifidobacterium pseudolongum. This leads to reduced inflammation in the colon, circulation and knee, and protection from OA. This novel recognition of a gut microbiome-OA connection sets the stage for discovery of new OA therapeutics targeting specific microbes inhabiting the intestinal space to inhibit disease pathology.
2018-06-22 | GSE98287 | GEO
Project description:BACKGROUND & AIMS: There is mounting evidence that microbes resident in the human intestine contribute to diverse alcohol-associated liver diseases (ALD) including the most deadly form known as alcoholic hepatitis (AH). However, mechanisms by which gut microbiota synergize with excessive alcohol intake to promote liver injury are poorly understood. Furthermore, whether drugs that selectively target gut microbial metabolism can improve ALD has never been tested. METHODS: We used liquid chromatography tandem mass spectrometry to quantify the levels of microbe and host choline co-metabolites in healthy controls and AH patients, and identified the metabolite trimethylamine (TMA) as a gut microbe-derived biomarker of AH. In subsequent studies, we treated mice with non-lethal mechanism-based bacterial choline TMA lyase inhibitors to blunt gut microbe-dependent production of TMA in the context of chronic ethanol administration. Indices of liver injury were quantified by complementary RNA sequencing, biochemical, and histological approaches. In addition, we examined the impact of ethanol consumption and TMA lyase inhibition on gut microbiome structure via 16S rRNA sequencing. RESULTS: We show the gut microbial choline metabolite trimethylamine (TMA) is elevated in AH patients, which is correlated with reduced hepatic expression of the TMA oxygenase flavin-containing monooxygenase 3 (FMO3). Provocatively, we find that small molecule inhibition of gut microbial choline TMA lyase activity protects mice from ethanol-induced liver injury. TMA lyase inhibitor-driven improvement in ethanol-induced liver injury is associated with distinct reorganization of the gut microbiome community and host liver transcriptome. CONCLUSIONS: The microbial metabolite TMA is a biomarker of AH, and blocking TMA production from gut microbes can blunt ALD in mice.
2021-03-31 | GSE157681 | GEO
Project description:Opioids such as morphine have many beneficial properties as analgesics, however, opioids may induce multiple adverse gastrointestinal symptoms. We have recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. However, it is unclear how opioids modulate the gut homeostasis. By using a mouse model of morphine treatment, we studied effects of morphine treatment on gut microbiome. We characterized phylogenetic profiles of gut microbes, and found a significant shift in the gut microbiome and increase of pathogenic bacteria following morphine treatment when compared to placebo. In the present study, wild type mice (C57BL/6J) were implanted with placebo, morphine pellets subcutaneously. Fecal matter were taken for bacterial 16s rDNA sequencing analysis at day 3 post treatment. A scatter plot based on an unweighted UniFrac distance matrics obtained from the sequences at OTU level with 97% similarity showed a distinct clustering of the community composition between the morphine and placebo treated groups. By using the chao1 index to evaluate alpha diversity (that is diversity within a group) and using unweighted UniFrac distance to evaluate beta diversity (that is diversity between groups, comparing microbial community based on compositional structures), we found that morphine treatment results in a significant decrease in alpha diversity and shift in fecal microbiome at day 3 post treatment compared to placebo treatment. Taxonomical analysis showed that morphine treatment results in a significant increase of potential pathogenic bacteria. Our study shed light on effects of morphine on the gut microbiome, and its role in the gut homeostasis.
2018-04-16 | E-MTAB-5546 | biostudies-arrayexpress
Project description:In order to understand the appropriate use of potentially beneficial Gram positive microbes through their introduction in the gut microbiome, it is necessary to understand the influence of individual bacteria on the host response system at a cellular level. In the present study we showed that lipopolysaccharide (LPS), flagellated Gram negative bacteria, potentially beneficial Gram positive bacteria and yeast interact differently with human intestinal enterocytes (IEC) with a custom-designed expression microarray evaluating 17 specific host-response pathways. Only, LPS and flagellated Gram negative bacteria induced inflammatory response, while a subset of Gram positive microbes had anti-inflammatory potential. The main outcome from the study was the differential regulation of the central MAPK signaling pathway by these Gram positive microbes versus commensal/pathogenic Gram negative bacteria. The microarray was efficient to highlight the impact of individual bacteria on IEC response, but q-RT-PCR validation demonstrated some underestimation for down regulated genes by the microarray. This Immune Array will allow us to better understand the mechanisms underlying pathogen-induced host immune responses, aid in the selection potentially probiotic microbes and perhaps select biomarkers for future clinical studies. In this study, human immune response was assessed by stimulating HT-29 intestinal epithelial cells (IEC) with different microorganisms (or LPS) individually. For each of the 12 different treatments, between 4 and 8 biological replicates were performed, analyzed with dye-swaps and hybridized against control or untreated cells. Genes that were showing a 1.3 mRNA transcript abundance fold change and a P-value below 0.05 were considered to be differentially expressed.
2011-12-31 | E-GEOD-31394 | biostudies-arrayexpress