Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1073028 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27880456_1.fastq.gz | Fastqsanger.gz | |||
| SRR27880456_2.fastq.gz | Fastqsanger.gz | |||
| SRR27880457_1.fastq.gz | Fastqsanger.gz | |||
| SRR27880457_2.fastq.gz | Fastqsanger.gz | |||
| SRR27880458_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 30 |
Similar Datasets
Project description:Gut microbiota and their metabolites influence host gene expression and physiological status through diverse mechanisms. Here we investigate how gut microbiota and their metabolites impact host's mRNA m6A epitranscriptome in various antibiotic-induced microbiota dysbiosis models. With multi-omics analysis, we find that the imbalance of gut microbiota can rewire host mRNA m6A epitranscriptomic profiles in brain, liver and intestine. We further explore the underlying mechanisms regulating host mRNA m6A methylome by depleting the microbiota with ampicillin. Metabolomic profiling shows that cholic acids are the main down-regulated metabolites with Firmicutes as the most significantly reduced genus in ampicillin-treated mice comparing to untreated mice. Fecal microbiota transplantations in germ-free mice and metabolites supplementations in cells verify that cholic acids are associated with host mRNA m6A epitranscriptomic rewiring. Collectively, this study employs an integrative multi-omics analysis to demonstrate the impact of gut microbiota dysbiosis on host mRNA m6A epitranscriptomic landscape via cholic acid metabolism.
2024-04-21 | GSE218001 | GEO
Project description:Gut microbiota and their metabolites influence host gene expression and physiological status through diverse mechanisms. Here we investigate how gut microbiota and their metabolites impact host′s mRNA m6A epitranscriptome in various antibiotic-induced microbiota dysbiosis models. With multi-omics analysis, we find that the imbalance of gut microbiota can rewire host mRNA m6A epitranscriptomic profiles in brain, liver and intestine. We further explore the underlying mechanisms regulating host mRNA m6A methylome by depleting the microbiota with ampicillin. Metabolomic profiling shows that cholic acids are the main down-regulated metabolites with Firmicutes as the most significantly reduced genus in ampicillin-treated mice comparing to untreated mice. Fecal microbiota transplantations in germ-free mice and metabolites supplementations in cells verify that cholic acids are associated with host mRNA m6A epitranscriptomic rewiring. Collectively, this study employs an integrative multi-omics analysis to demonstrate the impact of gut microbiota dysbiosis on host mRNA m6A epitranscriptomic landscape via cholic acid metabolism.
2024-04-21 | GSE216620 | GEO
Project description:Gut microbiota plays an important role during early development via bidirectional gut- brain signaling. We aimed to explore the potential link between gut microbiota/gut derived metabolites and sympathoadrenal stress responsivity
2018-11-25 | GSE122754 | GEO
Project description:The gut microbiota has been implicated in obesity and cardiometabolic diseases, although evidence in humans is scarce. We investigated how gut microbiota manipulation by antibiotics (7-day administration of amoxicillin, vancomycin, or placebo) affects host metabolism in 57 obese, prediabetic men. Vancomycin, but not amoxicillin, decreased bacterial diversity and reduced Firmicutes involved in short-chain fatty acid and bile acid metabolism, concomitant with altered plasma and/or fecal metabolite concentrations. Adipose tissue gene expression of oxidative pathways was upregulated by antibiotics, whereas immune-related pathways were downregulated by vancomycin. Antibiotics did not affect tissue-specific insulin sensitivity, energy/substrate metabolism, postprandial hormones and metabolites, systemic inflammation, gut permeability, and adipocyte size. Importantly, energy harvest, adipocyte size, and whole-body insulin sensitivity were not altered at 8-week follow-up, despite a still considerably altered microbial composition, indicating that interference with adult microbiota by 7-day antibiotic treatment has no clinically relevant impact on metabolic health in obese humans. This randomized, placebo-controlled, double-blind study had a 3-armed parallel design. Overweight/obese participants were randomized to oral intake of amoxicillin, vancomycin or placebo for 7 consecutive days. After an overnight fast, subcutaneous adipose tissue biopsies were taken that were subjected to gene expression profiling by array.
2016-07-15 | E-GEOD-76003 | biostudies-arrayexpress
Project description:The intestinal epithelium senses and responds to the myriad of signals from gut microbiota, but it remains unclear how these signals are integrated to drive physiological responses. In this work, we found that enterochromaffin (EC) cells in the gut serve as signal integration hubs for microbial metabolites. EC cells coordinate responses to combinations of microbial metabolites, resulting in complex alterations in serotonin signaling that drive changes in GI physiology. We found that microbial metabolites either directly trigger responses or alter the expression of receptors for other microbial metabolites in EC cells. The microbiota-derived purine derivative hypoxanthine triggers a signaling pathway by activating G-protein coupled receptor A1R, which in turn activates the calcium channel TRPC4, resulting in increased serotonin release and accelerated GI transit. On the other hand, bacteria-derived butyrate does not evoke EC cell calcium influx by itself, but drives epigenetic changes that upregulate TRPC4 expression, thereby enhancing response to metabolites like hypoxanthine and norepinephrine that act via TRPC4. Since the expression TRPC4 is limited to EC cells, these cells function as specialized epithelial sensors that integrate signals from regulatory (butyrate) and effector metabolites like hypoxanthine and norepinephrine. These findings offer new microbiota-driven therapeutic avenues for conditions associated with altered GI function.
2025-02-10 | GSE286305 | GEO
Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.
2024-03-20 | GSE261887 | GEO
Project description:The gut microbiota has been implicated in obesity and cardiometabolic diseases, although evidence in humans is scarce. We investigated how gut microbiota manipulation by antibiotics (7-day administration of amoxicillin, vancomycin, or placebo) affects host metabolism in 57 obese, prediabetic men. Vancomycin, but not amoxicillin, decreased bacterial diversity and reduced Firmicutes involved in short-chain fatty acid and bile acid metabolism, concomitant with altered plasma and/or fecal metabolite concentrations. Adipose tissue gene expression of oxidative pathways was upregulated by antibiotics, whereas immune-related pathways were downregulated by vancomycin. Antibiotics did not affect tissue-specific insulin sensitivity, energy/substrate metabolism, postprandial hormones and metabolites, systemic inflammation, gut permeability, and adipocyte size. Importantly, energy harvest, adipocyte size, and whole-body insulin sensitivity were not altered at 8-week follow-up, despite a still considerably altered microbial composition, indicating that interference with adult microbiota by 7-day antibiotic treatment has no clinically relevant impact on metabolic health in obese humans.
2016-07-15 | GSE76003 | GEO
Project description:The gut microbiota plays an important role in host health. Microbiota dysbiosis has been implicated in the global epidemic of Metabolic Syndrome (MetS) and could impair host metabolism by noxious metabolites. It has been well established that the gut microbiota is shaped by host immune factors. However, the effect of T cells on the gut microbiota is yet unknown. Here, we performed a metagenomic whole-genome shotgun sequencing (mWGS) study of the microbiota of TCRb-/- mice, which lack alpha/beta T cells.
2024-05-06 | GSE262397 | GEO
Project description:Gut microbiota is an unignored target in maintaining intestinal homeostasis due to its regulatory effects on intestinal health through multiple mechanisms, including enhancing intestinal barriers, modulating microbial diversity, secreting various metabolites, etc. Bacteriocins produced by probiotics have been gradually proved vital for intestinal diseases intervention, however, the corresponding mechanisms have received less attention and the whole story of their regulative activities are hard to be fully uncovered. The two-peptide Plantaricin NC8 (PLNC8), coded by gene plnc8, is a bacteriocin ubiquitously produced by Lactobacillus plantarum, has been regarded as the potential vital bacteriocin for the anti-inflammatory effects of Lactobacillus plantarum. This study exploited CRISPR-cas9 and prokaryotic gene overexpression techniques to construct the plnc8 strains for the anti-inflammatory mechanism investigation. Based on the metagenomics, transcriptomics and metabolomics analysis, the anti-enteritis mechanism of PLNC8 systematically in DSS-induced enteritis models were comprehensively revealed. PLNC8 induced alterations in the composition of gut microbiota composition, promoting the alterations of multiple probiotics such as Eubacterium plexicaudatum, Doreasp.5-2, Enterococcus cecorum and Prevotella oulorum. Besides, various metabolites produced by the gut microbiota were influenced, and the key metabolites of xanthine, hypoxanthine, and L-histidine were regulated via purine and histidine metabolic pathways. These metabolites further inhibited p38 MAPK phosphorylation of enterocytes induced by DSS. Ultimately, the intestinal barrier repairment and anti- enteritis were achieved, proving the anti-enteritis effects of PLNC8 via microbe-metabolites-enterocyte axis.
2024-08-20 | GSE274981 | GEO
Project description:Gut microbiota contributes to the regulation of host immune response and homeostasis. Bile acid (BA) derivatives from gut microbiota can affect the differentiation and function of the immune cells. However, it is incompletely clear for the regulation of BA metabolites in the macrophages. We here find that BA metabolites can regulate sensitivity of macrophages to LPS and or Gram-negative bacteria. BA derivatives could induce lncRNA57RIK expression through sphingosine-1-phosphate receptor 2 (S1PR2) in the macrophages of mice and humans, which play a critical role in Gram-negative bacteria mediated IL-1β maturation and pyroptosis of macrophages. This lncRNA57RIK could bind intracellular proteases caspase-4/11 with guanylate-binding protein 1 (GBP1) in the human and mice together to cause LPS mediated activation of caspase-4/11. Murine or human lncRNA57RIK knockout (KO) macrophages did not produce response(s) to LPS or gram negative bacteria. LncRNA57RIK KO mice had also reduced inflammatory responses to LPS or Salmonella typhimurium (S.T) infection. Taken together, gut microbiota derived BA metabolites mediated lncRNA57RIK is necessary for LPS induced caspase-4/11 activation.
2024-09-21 | GSE277195 | GEO