Gut microbiota in Chronic Kidney Disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB34855 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3589150_1.fastq.gz | Fastqsanger.gz | |||
| ERR3589150_2.fastq.gz | Fastqsanger.gz | |||
| ERR3589160_1.fastq.gz | Fastqsanger.gz | |||
| ERR3589160_2.fastq.gz | Fastqsanger.gz | |||
| ERR3589170_1.fastq.gz | Fastqsanger.gz |
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Project description:The interplay of gut microbiota with the kidney system, characteristic to reduced kidney function and increased concentrations of urea in gut; in turn increases bacterial urease activity and generation of uremic toxins. Knowledge on these underlying bidirectional molecular mechanisms is nevertheless still limited. In this exploratory study, fecal proteomics analysis was performed, to investigate this largely unexplored biological material as a source of relevant information reflecting the gut-kidney axis at protein level. Specifically, fecal suspension samples from patients with chronic kidney disease (CKD); CKD1 (n = 12) and CKD4 (n = 17) were analysed by high resolution LC-MS/MS. Protein identification was performed using both the human and bacterial UniProt RefSeq reviewed databases, identifying 701 and 1011 unique proteins, respectively. Differential expression analysis (CKD4/CKD1) revealed significance for human proteins previously associated with reduced saccharolytic fermentation, inflammation and CKD, including pancreatic alpha-amylase and galectin-3-binding protein. Significant changes in bacterial proteins such as glyceraldehyde-3-phosphate dehydrogenase, suggest differential butyrate synthesis in CKD4/CKD1. Quantitatively measured decrease of pancreatic alpha-amylase and butyrate in CKD4/CKD1, supported these hypotheses. In conclusion, this analysis highlighted the presence of inflammation and suggested reduced saccharolytic fermentation affecting butyrate synthesis pathways in later disease stages. Validation by a multi-omics analysis is planned.
2025-06-02 | PXD048778 | Pride
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.
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Project description:Renal failure is associated with accumulation of various solutes called Uremic toxins. Post transcriptional regulation related to Chronic kidney disease (CKD) have already been described as RNA based silencing with micro RNA or modifications of mRNA degradation. Until now, alternative splice modification was not mentioned in the course of CKD. However, CKD is associated with modification of gene expression. The aim of the study was to explore modification of the alternative splice pattern in the course in CKD. The expression level of individual exons expression in human fibroblast were compared after culture to 96 hours of uremic condition or control condition. Three independant experiments were performed
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Project description:End-stage renal disease (ESRD) is the final stage of chronic kidney disease, which is increasingly prevalent worldwide and is associated with the progression of cardiovascular disease (CVD). Indoxyl sulfate (IS) and p-cresyl sulfate (PCS), major uremic toxins, are major risk factors involved in the pathology of CVD via adverse effects on endothelial cells and immune cells. Thus, transcriptomic overview of uremic toxin-mediated genes in immune cells of ESRD patients is critical, but not yet fully known. We investigated the alteration of gene expressions and biological pathways mediated by major uremic toxins, in ESRD patients monocytes, via microarray analysis. To explore uremic toxin-related transcriptional profiling in ESRD patient-derived monocytes, purified monocytes from healthy controls were treated with IS or PCS for 24 hr, followed by conducting microarray on these samples.
2020-07-30 | GSE155325 | GEO
Project description:Abstract: Histones are small proteins that form the core of nucleosomes, around which eukaryotic DNA wraps to ultimately form the highly organized and compressed structure known as chromatin. The N-terminal tails of histones are highly modified, and the modification state of these proteins dictates whether chromatin is permissive or repressive to processes that require physical access to DNA, including transcription and DNA replication and repair. The enzymes that add and remove histone modifications are known to be exquisitely sensitive to endogenous small molecule metabolite availability. In this manner, chromatin can adapt to changes in environment, particularly diet-induced metabolic state. Importantly, gut microbiota contribute to robust host metabolic phenotypes, and produce a myriad of metabolites that are detectable in host circulation. Further, gut microbial community composition and metabolite production are regulated by host diet, as a major source of carbon and energy for the microbiota. While prior studies have reported robust host metabolic associations with gut microbiota, the mechanisms therein remain largely unknown. Here we demonstrate that microbial colonization regulates global histone acetylation and methylation in multiple host tissues including colon, adipose tissue, and liver. This regulatory relationship is altered by diet: a “Western-type” diet leads to a general suppression of the microbiota-dependent chromatin changes observed in a polysaccharide rich diet. Finally, we demonstrate that supplementation of germ-free mice with major products of gut bacterial fermentation (i.e., short-chain fatty acids acetate, propionate, and butyrate) is sufficient to recapitulate many of the effects of colonization on host epigenetic states. These findings have profound implications for understanding the complex functional interactions between diet, gut microbiota, and host health.
2016-11-23 | GSE81115 | GEO
Project description:Abstract: Histones are small proteins that form the core of nucleosomes, around which eukaryotic DNA wraps to ultimately form the highly organized and compressed structure known as chromatin. The N-terminal tails of histones are highly modified, and the modification state of these proteins dictates whether chromatin is permissive or repressive to processes that require physical access to DNA, including transcription and DNA replication and repair. The enzymes that add and remove histone modifications are known to be exquisitely sensitive to endogenous small molecule metabolite availability. In this manner, chromatin can adapt to changes in environment, particularly diet-induced metabolic state. Importantly, gut microbiota contribute to robust host metabolic phenotypes, and produce a myriad of metabolites that are detectable in host circulation. Further, gut microbial community composition and metabolite production are regulated by host diet, as a major source of carbon and energy for the microbiota. While prior studies have reported robust host metabolic associations with gut microbiota, the mechanisms therein remain largely unknown. Here we demonstrate that microbial colonization regulates global histone acetylation and methylation in multiple host tissues including colon, adipose tissue, and liver. This regulatory relationship is altered by diet: a “Western-type” diet leads to a general suppression of the microbiota-dependent chromatin changes observed in a polysaccharide rich diet. Finally, we demonstrate that supplementation of germ-free mice with major products of gut bacterial fermentation (i.e., short-chain fatty acids acetate, propionate, and butyrate) is sufficient to recapitulate many of the effects of colonization on host epigenetic states. These findings have profound implications for understanding the complex functional interactions between diet, gut microbiota, and host health.
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Project description:Human gut microbiota metabolites associated with pregnancy and lactation stages.
2022-02-21 | MSV000088880 | MassIVE
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Project description:Controlling the progression of chronic kidney disease (CKD) at an early stage is critical for reducing disease severity. A cross-sectional study of chronic kidney disease (CKD) patients at all stages with S. stercoralis infection found that helminth infection caused gut dysbiosis, which may be involved in CKD progression. Because of the variation of gut microbiome results with helminth infection, the cross-sectional study of 16S rRNA sequencing, therefore, is insufficient to draw valid conclusions and correct the effects of S. stercoralis on the early stages of CKD. Combination with other omics approach is warrant to be better understand the disease.
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Project description:Adenine and nephrectomy can be used to establish models of uremic cardiomyopathy in rodents. Although these two approaches cause similar phenotypes of heart, adenine may directly act on cardiomyocytes and lead to different molecular changes from nephrectomy-induced uremic cardiomyopathy. Transcriptome analysis on left ventricles showed 789 upregulated and 345 downregulated genes in mice with nephrectomy-induced uremic cardiomyopathy compared to control mice, while 432 upregulated and 155 downregulated genes in mice with adenine diet-induced uremic cardiomyopathy compared to control mice. Functional analysis revealed that these DEGs were involved in pathways related to immune inflammation, metabolic responses, and synaptic transmission. Further analysis demonstrated that nephrectomy-induced uremic cardiomyopathy has enhanced cell cycle process/extracellular matrix remodeling and suppressed fatty acid metabolism, whereas adenine diet-induced uremic cardiomyopathy only exhibits increased inflammatory response/extracellular matrix remodeling. Compared with nephrectomy-induced uremic cardiomyopathy, adenine diet-induced uremic cardiomyopathy showed improved oxidative phosphorylation, aerobic electron transport chain, and tricarboxylic acid cycle, and suppressed cell cycle-related process, indicating that adenine and its derivates may affect the process of chronic kidney induced cardiac changes.
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