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The effects of ELF-1 on gene expression profiles of colonic tissue in DSS colitis at single cell level

ABSTRACT: The effects of ELF-1 on gene expression profiles of colonic tissue in DSS colitis at single cell level

PROVIDER: PRJNA1121317 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29324710_1.fastq.gz	Fastqsanger.gz
	SRR29324710_2.fastq.gz	Fastqsanger.gz
	SRR29324711_1.fastq.gz	Fastqsanger.gz
	SRR29324711_2.fastq.gz	Fastqsanger.gz

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Transcription factor ELF-1 protects against colitis by maintaining intestinal epithelium homeostasis

Project description:Inflammatory bowel disease (IBD) is a chronic, relapsing, and remitting disease characterized by chronic inflammation in the gastrointestinal tract. The exact etiology and pathogenesis of IBD remain elusive. Although ELF-1 has been known to be highly expressed in epithelial cells for past twenty years, little is known about its function in epithelial cells and epithelial-related IBD. Here, we demonstrated that ELF-1 deficiency in mouse lead to exacerbated DSS-induced colitis, marked by inflammation dominated by neutrophil infiltration and activation of IL-17 signaling pathways in various immune cells, including Th17, ILC3, γδT and NKT cells. Bone marrow transfer experiments confirmed ELF-1 deficiency in non-hematopoietic cells intrinsically worsened DSS-induced colitis. On one hand, ELF-1 deficiency enhanced the production of pro-inflammatory chemokines in colonic epithelial cells, leading to extensive infiltration of neutrophils and other immune cells into the colonic mucosal tissue. On the other hand, ELF-1 directly regulated the expression of the Rack1 gene in colonic epithelial tissue, which has been proved to play critical roles in maintaining intestinal homeostasis. Altogether, ELF-1 plays a protective role in colitis by maintaining intestinal epithelium homeostasis.

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The effects of ELF-1 on gene expression profiles of colonic tissue in DSS colitis at single cell level

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Project description:The lack of suitable animal models reflecting chronically relapsing inflammation and tissue remodeling have hindered fibrosis research in inflammatory bowel diseases (IBD). This study investigated changes in connective tissue in a chronic murine model using different cycles of dextran sodium sulphate (DSS) to mimic the relapsing nature of the disease. We used whole gene expression arrays to study differences in colonic gene expression levels between acute and more chronic DSS colitis, Acute and chronic relapsing colonic inflammation was induced in C57BL6 female mice using several cycles of exposure to DSS in drinking water, followed by recovery phases. Total RNA, extracted from snap frozen colon from five mice per condition was used to analyze mRNA expression via Affymetrix Mouse Gene 1.0 ST arrays.

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Transcriptomic anlaysis of the early response of the colonic epithelium to colitis induction by dextran sodium sulfate (DSS)

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Chemical-induced colitis lowers mitochondrial bioenergetic function in the colonic epithelium with minimal impacts on the proteome

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Project description:Temporal transcriptional profiles of colonic tissue during DSS-induce colitis

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