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Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice

ABSTRACT: Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice

PROVIDER: PRJNA786581 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17111009.fastq.gz	Fastqsanger.gz
	SRR17111010.fastq.gz	Fastqsanger.gz
	SRR17111011.fastq.gz	Fastqsanger.gz
	SRR17111012.fastq.gz	Fastqsanger.gz
	SRR17111013.fastq.gz	Fastqsanger.gz

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Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ATAC_invivo]

Project description:Low-grade chronic inflammation is considered a hallmark of ageing and associated with impaired tissue function and development of disease. However, how cell-intrinsic and -extrinsic factors interact to establish this phenotype, termed inflammaging, remains poorly understood. We addressed this question in the mouse intestinal epithelium, using organoid cultures to dissect stem cell-intrinsic and -extrinsic sources of increased inflammatory signaling upon ageing. At the single-cell level, we found that inflammaging establishes differently in cells along the crypt-villus axis, including intestinal stem cells (ISCs). Importantly, the inflammaging phenotype was stably propagated by aged ISCs in organoid cultures and associated with increased chromatin accessibility of inflammation-associated loci in vivo and ex vivo, indicating a cell-intrinsic memory of inflammation. Mechanistically, we show that expression of inflammaging genes is dependent on STAT1 signaling. Together, our data reveal that inflammaging in the intestine is promoted by a cell-intrinsic mechanism, stably propagated by ISCs and associated with a disbalance in immune homeostasis.

2023-10-26 | GSE233898 | GEO

Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [Capture-C]

2023-10-26 | GSE233899 | GEO

Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ATAC_invivo]

Project description:Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ATAC_invivo]

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Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ATAC-Seq]

Project description:Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ATAC-Seq]

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Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [Capture-C]

Project description:Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [Capture-C]

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Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [single-cell RNA-seq]

Project description:Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [single-cell RNA-seq]

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Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [in vivo bulk RNA-Seq]

Project description:Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [in vivo bulk RNA-Seq]

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Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ex vivo bulk RNA-Seq]

Project description:Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ex vivo bulk RNA-Seq]

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Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ATAC-Seq]

Project description:During ageing, cell-intrinsic and extrinsic factors lead to the decline of tissue function and organismal health. Disentangling these factors is important for developing effective strategies to prolong organismal healthspan. Here, we addressed this question in the mouse intestinal epithelium, which forms a dynamic interface with its microenvironment and receives extrinsic signals affecting its homeostasis and tissue ageing. We systematically compared transcriptional profiles of young and aged epithelial cells in vivo and ex vivo in cultured intestinal organoids. We found that all cell types of the aged epithelium exhibit an inflammation phenotype, which is marked by MHC class II upregulation and most pronounced in enterocytes. This was accompanied by elevated levels of the immune tolerance markers PD-1 and PD-L1 in the aged tissue microenvironment, indicating dysregulation of immunological homeostasis. Intestinal organoids from aged mice still showed an inflammation signature after weeks in culture, which was concurrent with increased chromatin accessibility of inflammation-associated loci. Our results reveal a cell-intrinsic, persistent inflammation phenotype in aged epithelial cells, which might contribute to systemic inflammation observed during ageing.

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