Metagenome-wide analyses uncover gut bacterial signatures and implicate taxon-specific functions in end-stage renal disease
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ABSTRACT:
PROVIDER: PRJEB65297 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR11869200_1.fastq.gz | Fastqsanger.gz | |||
| ERR11869200_2.fastq.gz | Fastqsanger.gz | |||
| ERR11869300_1.fastq.gz | Fastqsanger.gz | |||
| ERR11869300_2.fastq.gz | Fastqsanger.gz | |||
| ERR11865801_1.fastq.gz | Fastqsanger.gz |
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Project description:BackgroundThe gut microbiota plays a crucial role in regulating host metabolism and producing uremic toxins in patients with end-stage renal disease (ESRD). Our objective is to advance toward a holistic understanding of the gut ecosystem and its functional capacity in such patients, which is still lacking.ResultsHerein, we explore the gut microbiome of 378 hemodialytic ESRD patients and 290 healthy volunteers from two independent cohorts via deep metagenomic sequencing and metagenome-assembled-genome-based characterization of their feces. Our findings reveal fundamental alterations in the ESRD microbiome, characterized by a panel of 348 differentially abundant species, including ESRD-elevated representatives of Blautia spp., Dorea spp., and Eggerthellaceae, and ESRD-depleted Prevotella and Roseburia species. Through functional annotation of the ESRD-associated species, we uncover various taxon-specific functions linked to the disease, such as antimicrobial resistance, aromatic compound degradation, and biosynthesis of small bioactive molecules. Additionally, we show that the gut microbial composition can be utilized to predict serum uremic toxin concentrations, and based on this, we identify the key toxin-contributing species. Furthermore, our investigation extended to 47 additional non-dialyzed chronic kidney disease (CKD) patients, revealing a significant correlation between the abundance of ESRD-associated microbial signatures and CKD progression.ConclusionThis study delineates the taxonomic and functional landscapes and biomarkers of the ESRD microbiome. Understanding the role of gut microbiota in ESRD could open new avenues for therapeutic interventions and personalized treatment approaches in patients with this condition.
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Project description:In this study, eighty tumor samples from 63 patients with renal cell carcinoma (RCC)-end-stage renal disease (ESRD) were analyzed by array comparative genomic hybridization (array CGH) using the Agilent Whole Human Genome 4×44K Oligo Micro Array. 79 tumor samples from 63 patients with RCC-ESRD
2012-03-24 | E-GEOD-28601 | biostudies-arrayexpress
Project description:Purpose: End-stage renal disease (ESRD) is a condition that is characterized by the loss of kidney function. ESRD patients suffer from various endothelial dysfunctions, inflammation, and immune system defects. Lysine malonylation (Kmal) is a recently discovered post-translational modification (PTM). Although Kmal has the ability to regulate a wide range of biological processes in various organisms, its specific role in ESRD is limited. Experimental design: In this study, the affinity enrichment and liquid chromatography-tandem mass spectrometry (LC-MS/MS) techniques have been used to create the first global proteome and malonyl proteome (malonylome) profiles of peripheral blood mononuclear cells (PBMCs) from twenty patients with ESRD and eighty-one controls. Results: On analysis, 793 differentially expressed proteins (DEPs) and 12 differentially malonylated proteins (DMPs) with 16 Kmal sites were identified. The Rap1 signaling pathway and platelet activation pathway were found to be important in the development of chronic kidney disease (CKD), as were DMPs TLN1 and ACTB, as well as one malonylated site. One conserved Kmal motif was also discovered. Conclusion: These findings provided the first report on the Kmal profile in ESRD, which could be useful in understanding the potential role of lysine malonylation modification in the development of ESRD.
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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). Despite accumulating evidence that monocytes/macrophages play a pivotal role in the pathogenesis of CVDs in ESRD patients, the current knowledge of transcriptomic signatures of monocytes or macrophages in ESRD patients is very lacking. Therefore, we investigated the transcriptome profiling of monocyte separated from patients with ESRD and HC. To explore the changes of gene expression in ESRD patient-derived monocytes, compared to monocytes from healthy controls, microarray were performed.
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Project description:Cardiovascular disease is the major cause of morbidity and death in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Patients with CKD and ESRD are at high risk for myocardial dysfunction, ischemia and heart failure. The mechanisms linking impaired renal function and increased risk for cardiovascular diseases, however, remain elusive. In addition, conventional therapeutics proven effective in reducing cardiovascular events in general population fail to provide similar benefits in uremic patients. There is a clear need to identify novel mediators of cardiovascular complications in uremic patients to provide insights into the pathogenesis, to tailor clinical care based on cardiovascular risks, and to develop new therapeutic strategies. It has become increasingly clear that the transcription of the eukaryotic genome is far more pervasive and complex than previously appreciated. While the expression of messenger RNAs (mRNAs) and microRNAs (miRNAs) account for only ~1% of all transcribed species, up to 90% of the mammalian genome is transcribed as long non-coding RNAs (lncRNAs), a heterogeneous group of non-coding transcripts longer than 200 nucleotides. LncRNAs have been shown to be functional and involved in specific physiological and pathological processes through epigenetic, transcriptional and post-transcriptional mechanisms. While the roles of lncRNAs in human diseases including cancer and neurodegenerative disorders are beginning to emerge, it remains unclear how lncRNA regulation contributes to cardiovascular complications in patients with renal dysfunction. In this proposal, we seek to apply next-generation sequencing technology to investigate circulating (plasma) lncRNA expression in control subjects and in patients with CKD and ESRD. We will test the hypothesis that circulating lncRNA expression signature can reflect the underlying kidney disease states in patients with CKD and ESRD. In addition, we will determine if circulating lncRNA expression signature could be a sensitive and specific biomarker to predict adverse cardiovascular events in patients with ESRD.
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Project description:Although an increase in studies has revealed the potential mechanisms underlying immune dysfunction during CKD progression, there are still many significant components that need to be clarified, such as the machinery of T-cell phenotype switching and the plasticity levels of different subsets. Fortunately, in the last decade, novel technologies such as single-cell RNA sequencing have enabled us to investigate transcriptomic profiles at the single-cell level and have enabled us to unravel the potential mechanisms of the heterogeneity of the cell phenotype underlying different diseases. In this study, we investigated the immune cell composition, function, and interaction with other cells in PBMCs (peripheral blood mononuclear cells) during the ESRD period, especially CD4+ T-cell plasticity and the involved signaling pathways and mediators, which could be potential therapeutic targets for preventing CKD progression and complications.
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