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Gut microbiota-derived butyrate robustly facilitates prenatal development and neurogenesis of enteric nervous system.

ABSTRACT: Gut microbiota-derived butyrate robustly facilitates prenatal development and neurogenesis of enteric nervous system.

PROVIDER: PRJNA1075648 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27944465_1.fastq.gz	Fastqsanger.gz
	SRR27944465_2.fastq.gz	Fastqsanger.gz
	SRR27944466_1.fastq.gz	Fastqsanger.gz
	SRR27944466_2.fastq.gz	Fastqsanger.gz
	SRR27944467_1.fastq.gz	Fastqsanger.gz

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Gut microbiota-derived butyrate robustly facilitates prenatal development and neurogenesis of enteric nervous system.

Project description:Our study demonstrates that the short-chain fatty acid, butyrate, greatly enhances the in utero development of ENCSCs and adult enteric neurogenesis, which was partially mediated through the receptors MCT1 and Ras signaling pathway. In conclusion, butyrate treatment may represent a potential therapy for various gastrointestinal motility disorders.

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Gene expression analysis following neurogenesis of adult enteric glia/progenitor cells

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A branching model of lineage differentiation underpinning the neurogenic potential of enteric glia (Single-cell expression analysis of small intestine enteric nervous system developmental data)

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Project description:The enteric nervous system (ENS) can control most essential gut functions owing to its organization into complete neural circuits consisting of a multitude of different neuronal subtypes. We used microarrays to identify transcription factor networks and signaling pathways involved in diversification and differentiation of enteric neurons during development of the enteric nervous system.

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Enteric glia express proteolipid protein 1 and are a transcriptionally unique population of glia in the mammalian nervous system

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Project description:Mental health profoundly impacts inflammatory responses in the body. This is particularly apparent in inflammatory bowel disease (IBD), where psychological stress is associated with disease flares. Here, we discover a critical role for the enteric nervous system (ENS) in mediating the aggravating effect of chronic stress on intestinal inflammation. We find that chronically elevated levels of glucocorticoids drive the generation of an inflammatory subset of enteric glia that promotes monocyte- and TNF-mediated colitis via CSF1. Additionally, glucocorticoids cause transcriptional immaturity in enteric neurons, acetylcholine deficiency, and dysmotility via TGFβ2. We verify the connection between the psychological state, intestinal inflammation, and dysmotility in two cohorts of human IBD patients. Together, these findings offer a mechanistic explanation for the impact of the brain on peripheral inflammation, define the ENS as a relay between psychological stress and gut inflammation, and suggest that stress management could serve as a valuable component of IBD care.

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The enteric nervous system relays psychological stress to intestinal inflammation [ScRNASeqCD45seq]

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