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Spatial and single cell transcriptomics reveals cellular crosstalk changes in ileal Crohn’s disease during inflammation

ABSTRACT: Spatial and single cell transcriptomics reveals cellular crosstalk changes in ileal Crohn’s disease during inflammation

PROVIDER: PRJNA949559 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23991100_1.fastq.gz	Fastqsanger.gz
	SRR23991100_2.fastq.gz	Fastqsanger.gz
	SRR23991101_1.fastq.gz	Fastqsanger.gz
	SRR23991101_2.fastq.gz	Fastqsanger.gz
	SRR23991102_1.fastq.gz	Fastqsanger.gz

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Spatial and single cell transcriptomics reveals cellular crosstalk changes in ileal Crohn’s disease during inflammation

Project description:Crohn’s disease is a lifelong disease with no cure that requires a better characterization of the cellular milieu and behavior that drives disease progression if more targeted therapies are to be developed. Our work with spatial and single cell transcriptomics adds new knowledge and gives spatial context to the cellular behavior and communication occurring within the intestinal mucosa during Crohn’s disease and how it is affected by inflammation.

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Microarray of formalin-fixed, paraffin-embedded uninvolved terminal ileal tissue obtained from ileo-colic resection surgeries of Crohn’s disease and control patients

Project description:The interpretation of transcriptional profiling studies of intestinal tissue from Crohn’s disease patients and control patients can be confounded by differing proportions of cell subsets (e.g. immune cells) present in these samples. In this study, we aimed to control for cellular composition using standard, archival formalin-fixed, paraffin-embedded (FFPE) tissue specimens from Crohn’s patients (n=36) and controls (n=32) who underwent intestinal resection surgery. This approach allowed us to use the same tissue specimens for histological screening to select study samples with similar cellular composition and for RNA extraction for RNA-seq transcriptional profiling. We hypothesized that this approach would allow us to more clearly identify molecular signatures in ileal tissue that were associated with Crohn’s disease-associated pathological mechanisms.

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Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [microarray]

Project description:Crohn’s disease is a chronic, debilitating inflammatory bowel disease. Here we report a critical role for phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3- deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was due to PLC-β3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/β-catenin signaling, which is essential for homeostasis and regeneration of the intestinal epithelium. PLC-β3 regulated the Wnt/β-catenin pathway in small intestinal epithelial cells (IECs) at transcriptional, epigenetic, and potentially protein-protein interaction levels. PLC-β3- deficient IECs were unable to respond to stimulation by R-spondin 1, an enhancer of Wnt/β-catenin signaling. Reduced expression of PLC-β3 and its signature genes was found in biopsies of ileal Crohn’s disease patients. PLC-β regulation of Wnt signaling was evolutionally conserved in Drosophila. Our data indicate that reduction of PLC-β3- mediated Wnt/β-catenin signaling contributes to the pathogenesis of ileal Crohn’s disease.

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Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [ATAC-Seq]

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Project description:Crohn’s disease (CD) is a debilitating gastrointestinal disorder that can impact the entirety of the GI tract. While substantial progress has been made in the medical management of CD, it remains incurable, frequently relapses, and is a significant financial and medical burden. The pathophysiology of CD is not well understood, but it is thought to arise in genetically susceptible individuals upon an environmental insult. Further elucidation of the disease etiology promises to expose additional therapeutic avenues, with the hope of reducing the burden of CD. One approach to understanding disease pathophysiology is to identify clinically relevant molecular disease subsets using transcriptomics. In this report, we use hierarchical clustering of the ileal transcriptomes of 34 patients to identify two CD subsets. Clinically, these clusters differed in the age of the patients at CD diagnosis, suggesting that age of disease onset impacts the pathophysiology of the disease. We found that the ileal transcriptomes of the early diagnosis cluster are enriched in inflammatory transcripts, including S100A9, which encodes a calprotectin subunit. Furthermore, levels of S100A9 distinguished individuals diagnosed before the age of 30 from those diagnosed after 30. Together, these findings suggest that medical management of CD patients should consider their age at diagnosis and therapeutic blockade of calprotectin may be beneficial in patients diagnosed earlier in life.

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