Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28427651_1.fastq.gz | Fastqsanger.gz | |||
| SRR28427651_2.fastq.gz | Fastqsanger.gz | |||
| SRR28427652_1.fastq.gz | Fastqsanger.gz | |||
| SRR28427652_2.fastq.gz | Fastqsanger.gz | |||
| SRR28427653_1.fastq.gz | Fastqsanger.gz |
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Project description:Gut microbiota and gallstone formation - cohousing study
2020-01-10 | E-MTAB-8550 | ExpressionAtlas
Project description:The gut microbiota promotes hepatic fatty acid desaturation and elongation in mice
2018-09-17 | E-MTAB-6079 | ExpressionAtlas
Project description:The understanding of the effects of compounds on the gut microbiome is limited and in particular we don’t know whether structurally similar compounds have similar or distinct effects on the gut microbiome. Here we selected berberine (BBR), an isoquinoline quaternary alkaloid, and sixteen structural analogues, and evaluated their effects on in vitro cultured individual gut microbiomes. The responses of the individual microbiomes were evaluated by metaproteomic profiles and by assessing butyrate production. BBR and eight analogues led to changes in proteins involved in microbial defense and stress responses, and enrichment of proteins from Verrumicrobia, Proteobacteria and Bacteroides phyla. It also led to a decrease in proteins from the Firmicutes phylum and its Clostridiales order which correlated to decrease proteins involved in the butyrate production pathway and butyrate concentration. Three of the compounds, Sanguinarine, Chelerythrine and Ethoxysanguinarine activated bacterial protective mechanisms, enriched Proteobacteria, increased opacity proteins and markedly reduced butyrate production. Dihydroberberine had a similar function to BBR in enriching the Akkermansia genus. In addition, it showed less overall adverse impacts on the functionality of the gut microbiome, including a better maintenance of the butyrate level. Our study shows that ex vivo microbiome assay can assess differential regulating effects of compounds with subtle differences and reveals that compound analogues can have distinct effects on the microbiome.
2020-07-21 | PXD015934 | Pride
Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress
Project description:Analysis of breast cancer survivors' gut microbiota after lifestyle intervention, during the COVID-19 lockdown, by 16S sequencing of fecal samples.
2023-01-13 | E-MTAB-12486 | biostudies-arrayexpress
Project description:Intracerebral hemorrhage (ICH) induces alterations in the gut microbiota composition, significantly impacting neuroinflammation post-ICH. However, the impact of gut microbiota absence on neuroinflammation following ICH-induced brain injury remain unexplored. Here, we observed that the gut microbiota absence was associated with reduced neuroinflammation, alleviated neurological dysfunction, and mitigated gut barrier dysfunction post-ICH. In contrast, recolonization of microbiota from ICH-induced SPF mice by transplantation of fecal microbiota (FMT) exacerbated brain injury and gut impairment post-ICH. Additionally, microglia with transcriptional changes mediated the protective effects of gut microbiota absence on brain injury, with Apoe emerging as a hub gene. Subsequently, Apoe deficiency in peri-hematomal microglia was associated with improved brain injury. Finally, we revealed that gut microbiota influence brain injury and gut impairment via gut-derived short-chain fatty acids (SCFA).
2024-05-13 | GSE266602 | GEO
Project description:The aim of this project was to explore the role of gut microbiota in the development of small intestine. The gut microbiota from different groups was used to treat the mice for 1 or 2 weeks. Then the small intestine samples were collected. The RNA was used for the RNA-seq analysis to search the role of gut microbiota in the development of small intestine. Groups: IMA100 mean gut microbiota from Alginate oligosaccharide 100mg/kg treated mice; IMA10 mean gut microbiota from Alginate oligosaccharide 10mg/kg treated mice; IMC mean gut microbiota from control group mice (dosed with water); Sa mean dosed with saline (no gut microbiota). "1" mean dosed for 1 week, "2" means dosed for 2 weeks.
2020-07-29 | GSE137999 | GEO
Project description:Objective: Benzbromarone (BBR) is an effective uric acid-lowering drug. However, it can induce severe liver damage in some patients. Studies have shown that BBR specifically exacerbates hepatic steatosis in obese individuals, leading to aggravated liver injury. The exact mechanism behind this phenomenon remains unclear. Methods: db/db mice were divided into four groups: Control, BBR administration (BBR), Pparg knockdown (Pparg-KD), and BBR administration with Pparg knockdown (BBR + Pparg-KD). One week after AAV8-shRNA-Pparg virus injection, mice were orally administered BBR for four weeks, and changes in blood glucose and body weight were measured. Subsequently, samples were collected, and plasma lipid levels, hepatic lipid content, and liver function parameters were determined. RNA-seq was performed to assess changes in the hepatic gene expression profile and analyze the protective effect of PPARγ knockdown on BBR-induced drug-induced liver injury. Results: Mice in the BBR group exhibited more severe levels of plasma lipids, hepatic lipids, and liver function parameters compared to the Control group. However, mice in the BBR + Pparg-KD group showed significant improvements in these indicators compared to the BBR group. Transcriptomic analysis revealed that BBR administration upregulated the expression of various lipid synthesis-related genes, primarily associated with the PPAR signaling pathway. Furthermore, PPARγ knockdown reversed the increased expression of these lipid synthesis genes. This suggests that PPARγ knockdown has a significant protective effect against BBR-induced drug-induced liver injury. Conclusion: Hepatocyte-specific knockdown of PPARγ can protect against BBR-induced exacerbation of hepatic steatosis and liver injury by inhibiting the promotion of lipid synthesis through PPARγ activation.
2025-01-29 | GSE274748 | GEO
Project description:The gut microbiota exerts profound influence on poultry immunity and metabolism through mechanisms that yet need to be elucidated. Here we used conventional and germ-free chickens to explore the influence of the gut microbiota on transcriptomic along the gut-lung axis in poultry. Our results demonstrated a differential regulation of genes associated with innate immunity and metabolism in the spleen of germ-free birds.
2024-08-28 | E-MTAB-14264 | biostudies-arrayexpress