Ontology highlight
ABSTRACT:
PROVIDER: PRJNA546529 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9206880_1.fastq.gz | Fastqsanger.gz | |||
| SRR9206880_2.fastq.gz | Fastqsanger.gz | |||
| SRR9206890_1.fastq.gz | Fastqsanger.gz | |||
| SRR9206890_2.fastq.gz | Fastqsanger.gz | |||
| SRR9206900_1.fastq.gz | Fastqsanger.gz |
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Project description:Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries. There is growing evidence that dysbiosis of the intestinal microbiota and disruption of microbiota-host interactions contribute to the pathology of NAFLD. We previously demonstrated that gut microbiota derived tryptophan metabolite indole-3-acetate (I3A) was decreased in both cecum and liver of high-fat diet-fed mice and attenuated the expression of inflammatory cytokines in macrophages and TNF-a and fatty acid induced inflammatory responses in an aryl-hydrocarbon receptor (AhR) dependent manner in hepatocytes. In this study, we investigated the effect of orally administered I3A in a mouse model of diet induced NAFLD. Western diet (WD)-fed mice given sugar water (SW) with I3A showed dramatically decreased serum ALT, hepatic TG, liver steatosis, hepatocyte ballooning, lobular inflammation, and hepatic production of inflammatory cytokines, compared to WD-fed mice given only SW. Metagenomic analysis show that I3A administration did not significantly modify the intestinal microbiome, suggesting that I3A’s beneficial effects likely reflect the metabolite’s direct actions on the liver. Administration of I3A partially reversed WD induced alterations of liver metabolome and proteome, notably, decreasing expression of several enzymes in hepatic lipogenesis and β- oxidation. Mechanistically, we also show that AMP-activated protein kinase (AMPK) mediates the anti-inflammatory effects of I3A in macrophages. The potency of I3A in alleviating liver steatosis and inflammation clearly demonstrates its potential as a therapeutic modality for preventing the progression of steatosis to NASH.
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Project description:The potential of orally administered colostrum-derived EVs to regulate gut microbiota dysbiosis and prevent non-alcoholic steatohepatitis was evaluated. The results demonstrated that colostrum-derived EVs improved steatosis, fibrosis, and inflammation. Transcriptome analysis showed decreased lipid metabolism, bacterial response, and inflammatory responses in the intestine, and reduced inflammatory and fibrosis-related pathways in the liver. Gut microbiota and metabolite analysis revealed an increased abundance of Akkermansia and elevated cholesterol excretion. Additionally, treatment with colostrum-derived EVs increased the production of tight junction proteins and mucin in the intestine. These findings suggest that increased Akkermansia due to colostrum-derived EVs improves intestinal inflammation and barrier function, preventing endotoxin translocation to the liver and thereby reducing liver inflammation and fibrosis.
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Project description:Ochratoxin A gene expression profiling in liver and kidney, with time points of exposure from 7 days to 12 months Experiment Overall Design: three replicates for each timepoint measured, control and ochratoxin A treated for both liver and kidney. <br><br>Note that files GSM62732.CEL and GSM62733.CEL, and files GSM62730.CEL and GSM62739.CEL as downloaded from GEO contain identical data.
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Project description:Inappropriate cross talk between mammals and their gut microbiota may trigger intestinal inflammation and drive extra-intestinal immune-mediated diseases. Studies with germ-free or gnotobiotic animals represent the gold standard for research on bacterial-host interaction but they are not readily accessible to the wide scientific community. We aimed at refining a protocol that in a robust manner would deplete murine intestinal microbiota and prove to have significant biologic validity. Previously published protocols for depleting mice of their intestinal microbiota by administering broad-spectrum antibiotics in drinking water were difficult to reproduce. We show that twice daily delivery of antibiotics by gavage depleted mice of their cultivable fecal microbiota and reduced the fecal bacterial DNA load by approximately 400 fold while ensuring the animals’ health. Mice subjected to the protocol for 17 days displayed enlarged ceca, reduced Peyer’s patches and small spleens. Antibiotic treatment significantly reduced the expression of antimicrobial factors and altered the expression of 517 genes in total in the colonic epithelium. Genes involved in cell cycle were significantly altered concomitant with reduced epithelial proliferative activity in situ assessed by Ki-67 expression, suggesting that commensal microbiota drives cellular proliferation in colonic epithelium. We present a robust protocol for depleting mice of their cultivatable intestinal microbiota with antibiotics by gavage and show that the biological effect of this depletion is phenotypic characteristics and epithelial gene expression profile similar to those of germ-free mice. Comparison of genome-wide gene expression of colon intestinal epithelial cells from mice subjected to microbiota depletion protocol against to control mice.
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