Ontology highlight
ABSTRACT:
PROVIDER: PRJEB20175 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1904810.fastq.gz | Fastqsanger.gz | |||
| ERR1904820.fastq.gz | Fastqsanger.gz | |||
| ERR1904830.fastq.gz | Fastqsanger.gz | |||
| ERR1904840.fastq.gz | Fastqsanger.gz | |||
| ERR1904850.fastq.gz | Fastqsanger.gz |
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Project description:Recovery of the gut microbiota in ampicillin-treated mice is dependent on the environment
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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 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.
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Project description:Adequate sleep is essential for relieving stress and rejuvenating the mind; however, undesirable physiological and pathological responses resulting from sleep insufficiency or sleep deprivation (SD) are becoming increasingly common. However, the influence of sleep deficiency on gut microbiota and microbiota-associated human diseases, especially on cardiac diseases remain controversial. Here, we constructed the experimental SD model in mice and found it significantly resulted in weakness, depression-like behaviors, and multiple organs dysfunction. Intriguingly, SD mice developed pathogenic cardiac hypertrophy and fibrosis with poor ejection fraction as well as fractional shortening. 16s rRNA sequencing demonstrated that SD-induced the pathogenic effects of gut microbiota, which was also observed in mice received by fecal microbe from SD mice in fecal microbiota transplantation (FMT) assays. Next, we investigated the therapeutic effects and underlying mechanisms of oxygen therapy in gut microbiota-associated cardiac fibrosis and dysfunction. The environment of 30% oxygen concentration effectively ameliorated the pathological effects on cardiac function. Transcriptome data also found oxygen therapy targeted several hypoxia-dependent pathways and suppressed cardiac collagen production. In conclusion, these results indicated the importance of sufficient sleep in gut microbiota and may represent a potential therapeutic strategy of oxygen environment exerts protective effects in sleepless sufferings through gut microbiota.
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Project description:Changes in the gut microbiome can have profound effects on the nervous system through modulation of T cell and microglia function. Since our prior studies demonstrated that T cells and microglia positively regulate low-grade glioma growth through the establishment of T cell-microglia immune circuit, we sought to explore the impact of changes in the gut microbiota on tumor biology. For these studies, genetically engineered Neurofibromatosis type 1 (NF1) optic glioma (Nf1-OPG) mice were raised in a germ-free environment or treated with antibiotics to deplete gut bacteria. First, we demonstrated that Nf1-OPG mice raised in a germ-free (gnotobiotic) environment or treated with specific antibiotics lacked optic gliomas and had improved OPG-induced retinal pathology (increased retinal nerve fiber layer thickness). Second antibiotic-treated Nf1-OPG mice gavaged with fecal microbiota from Nf1-OPG mice raised in a standard barrier facility restored optic glioma growth. Third, we showed that both germ-free and antibiotic-treated Nf1-OPG mice exhibited reduced intra-tumoral CD8+ T cell content resulting from decreased microglia chemokine production. Collectively, these findings establish a mechanistic relationship between the gut microbiota and brain tumor growth relevant to potential therapeutic interventions for pediatric low-grade gliomas.
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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.
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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.
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Project description:Mammalian species have co-evolved with intestinal microbial communities that can shape development and adapt to environmental changes, including antibiotic perturbation or nutrient flux. In humans, especially children, microbiota disruption is common, yet the dynamic microbiome recovery from early-life antibiotics is still uncharacterized. Using a mouse model mimicking pediatric antibiotic use, we found that therapeutic-dose pulsed antibiotic treatment (PAT) with a beta-lactam or macrolide altered both host and microbiota development. Early-life PAT accelerated total mass and bone growth, and resulted in progressive changes in gut microbiome diversity, population structure, and metagenomic content, with microbiome effects dependent on the number of courses and class of antibiotic. While control microbiota rapidly adapted to a change in diet, PAT slowed the ecological progression, with delays lasting several months in response to the macrolide. This study identifies key markers of disturbance and recovery, which may help provide therapeutic targets for microbiota restoration following antibiotic treatment. C57BL/6J mice received three antibiotic courses: at days 10-15, 28-31, and 37-40 of life, amoxicillin or tylosin.Livers were collected at age 22 weeks, RNA was extracted, and transcriptional differences were measured by microarray analysis.
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Project description:Most hospitalized preterm infants receive antibiotics (AB) in the first days of life to treat or prevent systemic infections. Short-term, early AB treatment may also prevent against the microbiota-dependent serious gut disorder, necrotising enterocolitis (NEC). However, it remains a challenge to predict or early detection of NEC in the first weeks of life and few diagnostic markers exist. Using preterm piglets as models for infants, we hypothesised that proteomic profiling could be used to identify new early plasma biomarkers of NEC with or without prior AB treatment. Preterm newborn pigs were treated with saline (CON) or antibiotics (ampicillin, gentamicin, and metronidazole), given enterally (ENT) or parenterally (PAR), and fed formula for four days to induce NEC. The gut was collected for scoring of NEC lesions and blood was collected for haematology and plasma proteomics
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