Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1227423 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32470200_1.fastq.gz | Fastqsanger.gz | |||
| SRR32470200_2.fastq.gz | Fastqsanger.gz | |||
| SRR32470300_1.fastq.gz | Fastqsanger.gz | |||
| SRR32470300_2.fastq.gz | Fastqsanger.gz | |||
| SRR32470201_1.fastq.gz | Fastqsanger.gz |
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Project description:Next-Generation-Sequencing (NGS) technologies have led to important improvement in the detection of new or unrecognized infective agents, related to infectious diseases. In this context, NGS high-throughput technology can be used to achieve a comprehensive and unbiased sequencing of the nucleic acids present in a clinical sample (i.e. tissues). Metagenomic shotgun sequencing has emerged as powerful high-throughput approaches to analyze and survey microbial composition in the field of infectious diseases. By directly sequencing millions of nucleic acid molecules in a sample and matching the sequences to those available in databases, pathogens of an infectious disease can be inferred. Despite the large amount of metagenomic shotgun data produced, there is a lack of a comprehensive and easy-use pipeline for data analysis that avoid annoying and complicated bioinformatics steps. Here we present HOME-BIO, a modular and exhaustive pipeline for analysis of biological entity estimation, specific designed for shotgun sequenced clinical samples. HOME-BIO analysis provides comprehensive taxonomy classification by querying different source database and carry out main steps in metagenomic investigation. HOME-BIO is a powerful tool in the hand of biologist without computational experience, which are focused on metagenomic analysis. Its easy-to-use intrinsic characteristic allows users to simply import raw sequenced reads file and obtain taxonomy profile of their samples.
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Project description:<p>Background & Aims: Alcoholic liver disease (ALD) is a major public health concern. Gut dysbiosis plays a critical role in its pathogenesis, yet the specific microbial and functional shifts driving ALD progression require further elucidation. This study aims to characterize these alterations and their mechanisms.</p><p>Methods: We recruited 28 male patients with alcoholic fatty liver (AFL), 22 with alcoholic cirrhosis (ALC), and 25 healthy male controls. Fecal samples were analyzed via shotgun metagenomic sequencing and targeted short-chain fatty acid (SCFA) metabolomics. Serum samples underwent untargeted metabolomics. Key findings were validated in mouse models through fecal microbiota transplantation (FMT), bacterial gavage, and integrated transcriptomic and metabolomic analyses.</p><p>Results: Metagenomic analysis revealed a depletion of SCFA-producing bacteria (e.g., Faecalibacterium prausnitzii, Fusicatenibacter saccharivorans) and an enrichment of enterotoxigenic Bacteroides fragilis (ETBF) in ALD patients. Fecal concentrations of acetate, propionate, and butyrate were significantly decreased and negatively correlated with serum ALT, AST, and GGT levels. Serum metabolomics identified a distinct profile in ALD, featuring elevated levels of metabolites such as 9,10-DHOME and reduced levels of specific lysophosphatidylcholines. Multi-omics integration suggested microbial regulation of ALD via bile acid and SCFA pathways. FMT from ALD patients exacerbated alcohol-induced liver injury in mice. Gavage with ETBF significantly worsened ALD phenotypes in mice, likely mediated by Bacteroides fragilis toxin (BFT)-induced gut barrier damage and inflammation. Mouse multi-omics further demonstrated that ETBF perturbation enhanced the tryptophan-kynurenine metabolic pathway and upregulated hepatic retinol metabolism, contributing to increased liver injury, inflammation, and fibrosis.</p><p>Conclusion: Gut dysbiosis characterized by the loss of beneficial SCFA producers and the rise of pathogenic ETBF is pivotal in ALD progression. ETBF exacerbates disease via toxin-driven barrier dysfunction and the dysregulation of tryptophan and retinol metabolic pathways, revealing novel mechanistic insights and potential therapeutic targets.</p>
2026-01-10 | MTBLS13649 | MetaboLights
Project description:<p>Background & Aims: Alcoholic liver disease (ALD) is a major public health concern. Gut dysbiosis plays a critical role in its pathogenesis, yet the specific microbial and functional shifts driving ALD progression require further elucidation. This study aims to characterize these alterations and their mechanisms.</p><p>Methods: We recruited 28 male patients with alcoholic fatty liver (AFL), 22 with alcoholic cirrhosis (ALC), and 25 healthy male controls. Fecal samples were analyzed via shotgun metagenomic sequencing and targeted short-chain fatty acid (SCFA) metabolomics. Serum samples underwent untargeted metabolomics. Key findings were validated in mouse models through fecal microbiota transplantation (FMT), bacterial gavage, and integrated transcriptomic and metabolomic analyses.</p><p>Results: Metagenomic analysis revealed a depletion of SCFA-producing bacteria (e.g., Faecalibacterium prausnitzii, Fusicatenibacter saccharivorans) and an enrichment of enterotoxigenic Bacteroides fragilis (ETBF) in ALD patients. Fecal concentrations of acetate, propionate, and butyrate were significantly decreased and negatively correlated with serum ALT, AST, and GGT levels. Serum metabolomics identified a distinct profile in ALD, featuring elevated levels of metabolites such as 9,10-DHOME and reduced levels of specific lysophosphatidylcholines. Multi-omics integration suggested microbial regulation of ALD via bile acid and SCFA pathways. FMT from ALD patients exacerbated alcohol-induced liver injury in mice. Gavage with ETBF significantly worsened ALD phenotypes in mice, likely mediated by Bacteroides fragilis toxin (BFT)-induced gut barrier damage and inflammation. Mouse multi-omics further demonstrated that ETBF perturbation enhanced the tryptophan-kynurenine metabolic pathway and upregulated hepatic retinol metabolism, contributing to increased liver injury, inflammation, and fibrosis.</p><p>Conclusion: Gut dysbiosis characterized by the loss of beneficial SCFA producers and the rise of pathogenic ETBF is pivotal in ALD progression. ETBF exacerbates disease via toxin-driven barrier dysfunction and the dysregulation of tryptophan and retinol metabolic pathways, revealing novel mechanistic insights and potential therapeutic targets.</p>
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