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Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [scRNA-seq]

ABSTRACT: Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [scRNA-seq]

PROVIDER: PRJNA1219193 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32230503_1.fastq.gz	Fastqsanger.gz
	SRR32230503_2.fastq.gz	Fastqsanger.gz
	SRR32230504_1.fastq.gz	Fastqsanger.gz
	SRR32230504_2.fastq.gz	Fastqsanger.gz
	SRR32230505_1.fastq.gz	Fastqsanger.gz

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Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [SI bulk RNA-seq]

Project description:Necrotizing enterocolitis (NEC) is a prevalent pediatric emergency characterized by the sudden onset of intestinal ischemia and necrosis resulting from hyperinflammation.The interactions between the bile acid receptor FXR with gut microbiota and mucosal immunity in early postnatal life, and its exact role in the pathogenesis of NEC, are unknown.Here we analyze the role of FXR in IECs under NEC.

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Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [ILC3s bulk RNA-seq]

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Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [IEC bulk RNA-seq]

Project description:Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [IEC bulk RNA-seq]

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Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [ILC3s bulk RNA-seq]

Project description:Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [ILC3s bulk RNA-seq]

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Blocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance [RNA-seq]

Project description:Group 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46−CCR6− (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.

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Blocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance [ATAC-Seq]

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Blocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance

Project description:<p>Group 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46CCR6 (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.</p>

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