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IBS multi-omics

ABSTRACT: Longitudinal multi-omics reveals subset-specific mechanisms underlying irritable bowel syndrome

PROVIDER: PRJEB37924 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4775530.fastq.gz	Fastqsanger.gz
	ERR4775540.fastq.gz	Fastqsanger.gz
	ERR4775550.fastq.gz	Fastqsanger.gz
	ERR4775560.fastq.gz	Fastqsanger.gz
	ERR4775570.fastq.gz	Fastqsanger.gz

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Longitudinal multi-omics reveals subset-specific mechanisms underlying irritable bowel syndrome

Project description:Longitudinal multi-omics reveals subset-specific mechanisms underlying irritable bowel syndrome

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Longitudinal multi-omics reveals subset-specific mechanisms underlying irritable bowel syndrome

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Project description:Increased numbers of mast cells and their products have been linked to symptom onset and severity in patients with chronic diarrhea and abdominal pain. Although mast-cell inhibition ameliorates clinical manifestations and reduces mucosal inflammation, underlying molecular mechanisms remain unknown. Experiment Overall Design: Diarrhea-irritable bowel syndrome (d-IBS) patients were studied at baseline, or 6 months after natural evolution (control) or oral cromoglycate treatment. Jejunal biopsies were subjected to chip analysis (Affymetrix Human Genome U133 Plus 2.0 GeneChips).

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Longitudinal multi-omics reveals subset-specific mechanisms underlying irritable bowel syndrome

Project description:The gut microbiome has been implicated in multiple human chronic gastrointestinal (GI) disorders. Determining its mechanistic role in disease has been difficult due to apparent disconnects between animal and human studies and lack of an integrated multi-omics view of disease-specific physiological changes. We integrated longitudinal multi-omics data from the gut microbiome, metabolome, host epigenome, and transcriptome in the context of irritable bowel syndrome (IBS) host physiology. We identified IBS subtype-specific and symptom-related variation in microbial composition and function. A subset of identified changes in microbial metabolites correspond to host physiological mechanisms that are relevant to IBS. By integrating multiple data layers, we identified purine metabolism as a novel host-microbial metabolic pathway in IBS with translational potential. Our study highlights the importance of longitudinal sampling and integrating complementary multi-omics data to identify functional mechanisms that can serve as therapeutic targets in a comprehensive treatment strategy for chronic GI diseases. Linked cross omic data sets:Microbiome sequencing data associated with this study are available in the European Nucleotide Archive (ENA): accession number <a href='https://www.ebi.ac.uk/ena/browser/view/PRJEB37924' rel='noopener noreferrer' target='_blank'>PRJEB37924</a> and <a href='https://www.ebi.ac.uk/ena/browser/view/PRJNA612180' rel='noopener noreferrer' target='_blank'>PRJNA612180</a>.

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