Ontology highlight
ABSTRACT:
PROVIDER: PRJNA383901 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5468280_1.fastq.gz | Fastqsanger.gz | |||
| SRR5468280_2.fastq.gz | Fastqsanger.gz | |||
| SRR5468290_1.fastq.gz | Fastqsanger.gz | |||
| SRR5468290_2.fastq.gz | Fastqsanger.gz | |||
| SRR5468300_1.fastq.gz | Fastqsanger.gz |
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Project description:The gut microbiome is known to be sensitive to changes in the immune system, especially during autoimmune diseases such as Multiple Sclerosis (MS). Our study examines the changes to the gut microbiome that occur during Experimental Autoimmune Encephalomyelitis (EAE), an animal model for MS. We collected fecal samples at key stages of EAE progression and quantified microbial abundances with 16S V4 amplicon sequencing. Our analysis of the data suggests that commensal Lactobacillaceae fall in abundance during EAE while other commensal populations belonging to the Clostridiaceae, Ruminococcaceae, and Peptostreptococcaceae families expand. Community analysis with microbial co-occurrence networks points to these three taxa as mediators of gut microbiome dysbiosis. We also employed PICRUSt2 to impute MetaCyc Enzyme Consortium (EC) pathway abundances from the original microbial abundance data. From this analysis, we found that a number of imputed EC pathways responsible for the production of compounds with indole groups are enriched in mice undergoing EAE. Our analysis and interpretation of results provides a detailed picture of the changes to the gut microbiome that are occurring throughout the course of EAE disease progression.
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