Ontology highlight
ABSTRACT:
PROVIDER: PRJNA338475 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4036640_1.fastq.gz | Fastqsanger.gz | |||
| SRR4036640_2.fastq.gz | Fastqsanger.gz | |||
| SRR4036650_1.fastq.gz | Fastqsanger.gz | |||
| SRR4036650_2.fastq.gz | Fastqsanger.gz | |||
| SRR4036660_1.fastq.gz | Fastqsanger.gz |
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Project description:Our study confirms that gut microbiota is essential for motor dysfunction and neuropathology in LRRK2 G2019S mice. Monoculturing Parabacteroides goldsteinii mitigates age-related motor dysfunction, alpha-synuclein expression, neuroinflammation, and dopaminergic degeneration. Its effects on the gut microenvironment include suppressing the toll-like receptor 4 signaling pathway, facilitating the differentiation of intestinal dendritic cells and macrophages, and promoting anti-inflammatory intraepithelial CD4+ CD8αα+ T cells. It also upregulates tissue repair and immune differentiation pathways, enhances intestinal epithelial junction and mitochondrial function genes, and reduces colonic alpha-synuclein levels.
2025-08-01 | GSE283666 | GEO
Project description:Mitochondrial diseases progressively lead to multisystemic failure with treatment options remaining extremely limited. To investigate novel strategies that alleviate mitochondrial dysfunction, we have generated a tamoxifen-inducible, knockout mouse model of mitochondrial transcription factor A (TFAM), a nuclear-encoded protein involved in mitochondrial DNA (mtDNA) maintenance, under the control of the ubiquitin gene promoter — Tfamfl/flUbCre‑ERT2 (iTfamKO) mice. Systemic TFAM deficiency triggers mitochondrial decline in a myriad of tissues in adult mice. Consequently, iTfamKO mice manifest multiorgan dysfunction including lipodystrophy, sarcopenia, metabolic alterations, kidney failure, neurodegeneration, and locomotor dysregulation, which result in the premature death of these mice. Interestingly, iTfamKO mice display intestinal barrier disruption and gut dysbiosis, with diminished levels of microbiota-derived short-fatty acids (SCFAs), such as butyrate. Mice with a deficient proof-reading version of the mtDNA polymerase gamma (mtDNA-mutator mice) phenocopy the dysfunction of the intestinal barrier and bacterial dysbiosis with reduced levels of butyrate, suggesting that different mouse models of mitochondrial dysfunction share deficient generation of butyrate. Transfer of microbiota from healthy control mice or administration of tributyrin (TB), a butyrate precursor, delay multiple signs of multimorbidity extending lifespan in iTfamKO mice. Mechanistically, butyrate supplementation recovers epigenetic histone acylation marks that are lost in the intestine of Tfam deficient mice. Overall, our findings highlight the relevance of preserving host-microbiota symbiosis in disorders related to mitochondrial dysfunction.
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Project description:Irritable Bowel Syndrome (IBS) is a disorder of the gut-brain axis, characterized by altered gut function and frequent psychiatric co-morbidity. Although altered intestinal microbiome profiles have been documented, their relevance to the clinical expression of IBS is unknown. To evaluate a functional role of the microbiota, we colonized germ-free mice with fecal microbiota from healthy controls or IBS patients with accompanying anxiety, and monitored gut function and behavior. Mouse microbiota profiles clustered according to their human donors. Despite having taxonomically similar composition as controls, mice with IBS microbiota had distinct serum metabolomic profiles related to neuro- and immunomodulation. Mice with IBS, but not control microbiota, exhibited faster gastrointestinal transit, intestinal barrier dysfunction, innate immune activation and anxiety-like behavior. These results support the notion that the microbiota contributes to both intestinal and behavioral manifestations of IBS and rationalize the use of microbiota-directed therapies in ameliorating IBS.
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Project description:Alterations in composition and function of the intestinal microbiota have been observed in organismal aging across a broad spectrum of animal phyla. Recent findings, which have been derived mostly in simple animal models, have even established a causal relationship between age-related microbial shifts and lifespan, suggesting microbiota-directed interventions as a potential tool to decelerate aging processes. To test whether a life-long microbiome rejuvenation strategy could delay or even prevent aging in mammals, we performed recurrent fecal microbial transfer (FMT) in mice throughout life. Transfer material was either derived from 8-week-old mice (young microbiome, yMB) or from animals of the same age as the recipients (isochronic microbiome, iMB) as control. Physiological responses were analyzed by rotarod and a grip strength test, intestinal barrier function by FITC gavage and LAL assay, transcriptional responses by single cell RNA sequencing and microbiome function by 16S profiling and metagenomics. Colonization with yMB improved coordination and intestinal permeability compared to iMB. yMB encoded fewer pro-inflammatory factors and altered metabolic pathways favoring oxidative phosphorylation. Ecological interactions among bacteria in yMB were more antagonistic than in iMB hinting at more stable microbiome communities. Single cell RNA sequencing analysis of intestinal mucosa revealed a salient shift of cellular phenotypes in the yMB group with markedly increased ATP synthesis and mitochondrial pathways in enterocytes and TA cells but reduced inflammatory signaling in macrophages. Taken together, we demonstrate that life-long and repeated transfer of microbiota material from young mice improved age-related processes including motor coordination, intestinal permeability and immune cell phenotypes.
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Project description:Alterations in composition and function of the intestinal microbiota have been observed in organismal aging across a broad spectrum of animal phyla. Recent findings, which have been derived mostly in simple animal models, have even established a causal relationship between age-related microbial shifts and lifespan, suggesting microbiota-directed interventions as a potential tool to decelerate aging processes. To test whether a life-long microbiome rejuvenation strategy could delay or even prevent aging in mammals, we performed recurrent fecal microbial transfer (FMT) in mice throughout life. Transfer material was either derived from 8-week-old mice (young microbiome, yMB) or from animals of the same age as the recipients (isochronic microbiome, iMB) as control. Physiological responses were analyzed by rotarod and a grip strength test, intestinal barrier function by FITC gavage and LAL assay, transcriptional responses by single cell RNA sequencing and microbiome function by 16S profiling and metagenomics. Colonization with yMB improved coordination and intestinal permeability compared to iMB. yMB encoded fewer pro-inflammatory factors and altered metabolic pathways favoring oxidative phosphorylation. Ecological interactions among bacteria in yMB were more antagonistic than in iMB hinting at more stable microbiome communities. Single cell RNA sequencing analysis of intestinal mucosa revealed a salient shift of cellular phenotypes in the yMB group with markedly increased ATP synthesis and mitochondrial pathways in enterocytes and TA cells but reduced inflammatory signaling in macrophages. Taken together, we demonstrate that life-long and repeated transfer of microbiota material from young mice improved age-related processes including motor coordination, intestinal permeability and immune cell phenotypes.
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Project description:The role of environmental factors and gender disparities as determinants of health is incontrovertible. In the digestive sphere, it is noteworthy that one of the most prevalent diseases such as irritable bowel syndrome (IBS) has a predominance in females. The origin of IBS is related to mucosal microinflammation phenomena, psychosocial stress, and in the last years, alterations in gut microbiota. Recent observations from our group in healthy subjects, demonstrate that both chronic psychosocial stress, and female gender per se determine a significant intestinal epithelial barrier dysfunction in response to intercurrent stimuli, which, in susceptible individuals, could result in an early stage in the development of more lasting changes and the onset of clinical manifestations of IBS. Although the intimate mechanisms involved in stress-induced intestinal pathophysiology are not well known, diverse studies suggest that gut microbiota alteration, through epigenetic modifications of the main stress-mediators could be one of them. However, solid scientific evidence demonstrating the influence of stress on gut microbiota and epigenetics of the main stress-mediators is missing. Therefore, we want to investigate and characterize gender-dependent epigenetic modifications involved in intestinal barrier dysfunction in response to acute stress. The identification of gender-dependent abnormal epigenetic patterns related to female gender dysfunction can make a breakthrough in the understanding of the pathophysiology of the regulation of intestinal permeability, and promote positive diagnostic and therapeutic future progress in IBS.
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2024-12-26 | GSE285291 | GEO