Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1114405 | ENA |
REPOSITORIES: ENA
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Project description:Interleukin-10 deficiency suppresses colorectal cancer metastasis by enriching gut Parabacteroides distasonis
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Project description:RNA-seq: Interleukin-10 deficiency suppresses colorectal cancer metastasis by enriching gut Parabacteroides distasonis
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Project description:The mammalian gastrointestinal tract contains a diverse ecosystem of microbial species collectively making up the gut microbiome. Emerging evidence highlights a critical relationship between gut microbiota and neurocognitive development. Consumption of unhealthy yet palatable dietary factors associated with obesity and metabolic dysfunction (e.g., saturated fat, added sugar) produces microbiota dysbiosis and negatively impacts neurocognitive function, particularly when consumed during early life developmental periods. Here we explore whether excessive early life consumption of added sugars negatively impacts neurocognitive development via the gut microbiome. Using a rodent model of habitual sugar-sweetened beverage (SSB) consumption during the adolescent stage of development, we first show that excessive early life sugar intake impairs hippocampal-dependent memory function when tested during adulthood while preserving other neurocognitive domains. Gut microbiome genomic sequencing analyses reveal that early life SSB consumption alters the abundance of various bacterial populations, including elevations in operational taxonomic units within the genus Parabacteroides (P. distasonis and P. johnsonii) whose abundance negatively correlated with memory task performance. Additional results reveal that in vivo Parabacteroides enrichment of cultured P. distasonis and P. johnsonii bacterial species in adolescent rats severely impairs memory function during adulthood. Hippocampus transcriptome analyses identify gene expression alterations in neurotransmitter synaptic signaling, intracellular kinase signaling, metabolic function, neurodegenerative disease, and dopaminergic synaptic signaling-associated pathways as potential mechanisms linking microbiome outcomes with memory impairment. Collectively these results identify microbiota dysbiosis as a mechanism through which early life unhealthy dietary patterns negatively impact neurocognitive outcomes.
2021-02-25 | GSE150091 | GEO
Project description:Multiple sclerosis (MS) is a chronic inflammatory, demyelinating disease of the central nervous system. The pathogenesis of MS and other autoimmune diseases is defined by a disrupted equilibrium between IL-17A-producing CD4 T cells (Th17) and regulatory CD4 T cells (Treg). The development of Treg and Th17 cells can be regulated by the gut microbiota, however, it is unclear how the gut microbiota is impacted by IL-17A and how this, in turn, modulates Treg and disease. Here, we show that IL-17A deficiency promotes interferon-I-related gene expression and expands gut microbes that induce the Treg cells, resulting in milder disease in a mouse model of MS. Utilizing HLA-DR3.IL17A-/- transgenic mice, we showed significant enrichment of Treg-promoting gut microbes such as Prevotella sp. MGM1, Parabacteroides distasonis and Bacteroides sartorii species. Further, we observed enrichment of bacterial-specific short-chain fatty acid metabolic pathways that promote Treg function in HLA-DR3.IL17A-/- transgenic mice. Notably, disease severity was reversed in IL-17A sufficient mice that received fecal transplants from, and cohoused with, IL-17A-deficient mice, highlighting a critical role for the gut microbiota in inducing Treg and reducing disease severity. Collectively, we show that IL-17A is an important regulator of the gut microbiota-Treg axis, which mediates immune homeostasis, inflammation, and diseases such as MS.
2025-10-01 | GSE190048 | GEO
Project description:Parabacteroides distasonis Metagenome
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Project description:Outer membrane vesicles of Parabacteroides distasonis
2024-04-15 | PXD051464 |
Project description:Parabacteroides distasonis Genome sequencing
| PRJNA1064251 | ENA