Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1307064 | ENA |
REPOSITORIES: ENA
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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 dysbiosis characterizes systemic metabolic alteration, yet its causality is debated. To address this issue, we transplanted antibiotic-free conventional wild-type mice with either dysbiotic (“obese”) or eubiotic (“lean”) gut microbiota and fed them either a NC or a 72%HFD. We report that, on NC, obese gut microbiota transplantation reduces hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non-transplanted mice. Of note, this phenotype is blunted in conventional NOD2KO mice. By contrast, lean microbiota transplantation did not affect hepatic gluconeogenesis. In addition, obese microbiota transplantation changed both gut microbiota and microbiome of recipient mice. Interestingly, hepatic gluconeogenesis, PEPCK and G6Pase activity were reduced even once mice transplanted with the obese gut microbiota were fed a 72%HFD, together with reduced fed glycaemia and adiposity compared to non-transplanted mice. Notably, changes in gut microbiota and microbiome induced by the transplantation were still detectable on 72%HFD. Finally, we report that obese gut microbiota transplantation may impact on hepatic metabolism and even prevent HFD-increased hepatic gluconeogenesis. Our findings may provide a new vision of gut microbiota dysbiosis, useful for a better understanding of the aetiology of metabolic diseases. all livers are from NC-fed mice only.
2017-03-16 | GSE81318 | GEO
Project description:This study investigated the impact of a high cellulose diet (HCD) on intestinal homeostasis and food allergy development in BALB/c mice. While soluble fibers are known to mitigate FA via short-chain fatty acid (SCFA) production, the role of insoluble fibers like cellulose remains unclear. Mice fed HCD exhibited gut dysbiosis, characterized by increased Proteobacteria, decreased tight junction protein expression, and intestinal barrier impairment, despite unchanged SCFA levels. RNA sequencing revealed HCD-induced upregulation of immune pathways, including the positive regulation of B and T cells differentiation and antigen receptor-mediated signaling pathway. Following ovalbumin (OVA) sensitization, HCD-fed mice displayed exacerbated allergic symptoms, including elevated OVA-specific IgE, IgG, histamine, and mMCP-1 levels. Gut microbiota analysis highlighted enrichment of potentially pathogenic taxa in HCD+OVA groups. Fecal microbiota transplantation (FMT) from HCD donors to antibiotic-treated recipients showed severe food allergy responses, confirming microbiota-mediated effects. These findings demonstrate that HCD exacerbates food allergy through gut microbial dysbiosis, intestinal barrier disruption, and intestinal immune disorder.
2025-06-17 | GSE299687 | GEO
Project description:The period from birth to two years is the phase of the fastest growth and development in children, as well as an important window for the development of intestinal microbiota. Dysbiosis of the gut microbiome can lead to various adverse conditions in children, including malabsorption and immune abnormalities, ultimately resulting in a series of negative events related to growth and development. Lysine acetylation, as a significant post-translational modification, plays a complex and crucial role in the regulation of gut microbiota. This study aims to investigate the mechanism by which ABX-induced lysine acetylation affects the abnormal physiological state simulating gut microbiota dysbiosis in children. In this study, we identified a total of 16,579 acetylation sites from 5,218 proteins. We found that antibiotic-induced dysbiosis in young mice (3 weeks) can cause extensive changes in the lysine acetylation and proteomic profiles of cecal tissue. Differentially acetylated proteins are involved in various metabolic pathways, including the citrate cycle (TCA) cycle, butanoate metabolism, pyruvate metabolism, glycolysis/gluconeogenesis, and fatty acid biosynthesis. These differential acetylation sites are distributed across the cytoplasm, nucleus, and mitochondria, suggesting that multiple cellular functions are involved in regulation. Our findings suggest that early-life gut microbiota dysbiosis may lead to a series of metabolic disorders by regulating lysine acetylation in cecal tissue, resulting in delayed growth and development. This study aims to provide valuable insights into the molecular mechanisms underlying a series of pathophysiological processes caused by early-life gut microbiota dysbiosis. It contributes to a deeper understanding of the consequences of acetylation changes associated with early-life gut microbiota dysbiosis and its potential role in metabolic disorders.
2025-09-15 | PXD064558 | Pride
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.
2022-11-08 | PXD038036 |
Project description:The larynx is essential for swallowing, breathing, coughing, and voice production, supported by its unique microbial and immunological environment. Our previous research highlighted the role of resident laryngeal microbiota in shaping local immune responses. With growing interest in the gut-lung axis—the bidirectional communication between gut and respiratory immunity—the potential influence of gut microbiota on laryngeal immunity warrants exploration. We hypothesized that a gut-larynx axis may exist, where both resident laryngeal and gut microbiota contribute to immune modulation in the larynx. To investigate this, we treated conventionally raised, wild-type C57BL/6J mice with an oral antibiotic regimen known to disrupt gut microbiota, comparing them to untreated controls. Following treatment, the gut microbiota was significantly disrupted, while the laryngeal microbiota remained largely unchanged. However, antibiotic-treated mice exhibited marked changes in epithelial and immune cell proportions, as well as fibroblasts. Differential gene expression across cell types highlighted pathways related to epithelial barrier integrity, immune signaling, and bacterial response. Additionally, gut dysbiosis affected gene regulatory networks, with the activity of regulons Etv4(+), Irf3(+), Hltf(+), Mga(+), and Nfil3(+) showing significant changes. Notably, cell-cell communication was also altered, especially in immune-epithelial interactions, with integrin-mediated signaling emerging as a key ligand-receptor pathway in these intercellular communications. These findings suggest that gut and laryngeal microbiota may work synergistically to modulate immune responses in the larynx, underscoring the importance of considering gut-larynx interactions in studies of respiratory immunity.
2025-03-04 | GSE290718 | GEO
Project description:Intestinal microbiota dysbiosis is related to many metabolic diseases in human health. Meanwhile, as an irregular environmental light-dark cycle, short-day (SD) may induce host circadian rhythms disturbances and worsen the risks of gut dysbiosis. Herein, we investigated how LD cycles regulate intestinal metabolism upon the destruction of gut microbes with antibiotic treatments. The transcriptome data indicated that SD have some negative effects on hepatic metabolism, endocrine, digestive, and diseases processes compared with normal light-dark cycle (NLD).The SD induced epithelial and hepatic purine metabolism pathway imbalance in ABX mice, the gut microbes, and their metabolites, all of which could contribute to host metabolism and digestion, endocrine system disorders, and may even cause diseases in the host.
2022-05-26 | GSE203566 | GEO
Project description:DNA methylation profile of mouse sperm from conventionally-raised mice and gut dysbiosis experienced mice were characterized using whole-genome bisulfite sequencing. Genome-wide DNA methylation changes between control and dysbiotic male�s sperm were highly comparable, with no change in DNAme globally or at genomic features, only 21 differentially methylated regions (DMR) were identified, which did not overlap known regulatory elements. Epididymal sperm samples were harvested from 11 weeks old inbred male mice that were experiencing gut microbiota dysbiosis for 6-week (antibiotics treated, n=5), or drink sterilized water (control, n=5).
2023-11-13 | E-MTAB-10033 | biostudies-arrayexpress
Project description:Periodontitis is increasingly linked to diverse brain disorders, yet causal mechanisms remain elusive. Here we demonstrate that ligature-induced oral dysbiosis in mice is sufficient to perturb central function. Six weeks of periodontitis produced anxiety-like behavior and motor deficits, accompanied by microglial depletion, reduced neuronal activity and region-selective transcriptional down-regulation in the frontal cortex. Pharmacological microglial ablation phenocopied, and glucocorticoid-receptor blockade rescued, these abnormalities, implicating microglia and activation of the hypothalamic–pituitary–adrenal axis. 16S rRNA gene sequencing revealed significant shifts in oral and gut microbiota that were partially normalized by a broad-spectrum antibiotic cocktail. Antibiotics alone elevated corticosterone but did not affect microglia or behavior, indicating that dysbiosis and glucocorticoids act synergistically on the brain dysfunction. Antibiotic treatment restored microglial density and behaviors in ligature mice, despite plasma corticosterone levels remaining elevated and comparable to those in antibiotic-treated controls. Our findings suggest oral dysbiosis as a tractable driver of neuroimmune dysfunction and redefine periodontitis as a systemic disorder with direct consequences for brain health.
2025-08-28 | GSE299912 | GEO