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Ileal S100A9 expression distinguishes Crohn’s disease patients by age at diagnosis

ABSTRACT: Ileal S100A9 expression distinguishes Crohn’s disease patients by age at diagnosis

PROVIDER: PRJNA636953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11914854.fastq.gz	Fastqsanger.gz
	SRR11914854_1.fastq.gz	Fastqsanger.gz
	SRR11914854_2.fastq.gz	Fastqsanger.gz
	SRR11914855.fastq.gz	Fastqsanger.gz
	SRR11914855_1.fastq.gz	Fastqsanger.gz

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Ileal S100A9 expression distinguishes Crohn’s disease patients by age at diagnosis

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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Project description:Based on genetic risk factors and natural history, Crohn’s disease (CD) can be separated in two entities, an ileal and a colonic disease. Protein based-approaches are needed to elucidate whether such subphenotypes are related to distinct pathophysiological processes. In this work, we compared the proteome of ulcer edge to the one of paired control tissue in ileum and colon of CD patients. We revealed that ileal and colonic ulcer edge can be distinguished by a differential distribution of epithelial–mesenchymal transition proteins, neutrophil degranulation proteins and ribosomal proteins. In ileal and colonic ulcer edge, we found a quasi-systematic increase of the proteins implicated in the pathway of protein processing in endoplasmic reticulum and a quasi-systematic decrease of mitochondrial proteins. Our study provides for the first time protein-based evidences showing partly distinct pathophysiological processes associated to ileal and colonic ulcer edge in CD. This could constitute a first step toward the development of gut segment-specific diagnostic markers and therapeutics.

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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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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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A distinct epigenetic profile distinguishes stenotic from non-inflamed fibroblasts in the ileal mucosa of Crohn's disease patients [methylation]

Project description:The Illumina Infinium EPIC Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 867,000 CpGs in ileal fibroblast samples. Samples included 5 control samples and 13 Crohn’s disease samples. The Crohn’s disease samples can be further subdivided into inflamed (2), non-inflamed (7) and stenotic (4) samples. This experiment together was performed in conjunction with a gene expression experiment (GSE99816). Use Supplemental Table 2 of the manuscript to quickly find the samples that were present in both experiments.

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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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Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [16S rRNA]

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-3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/-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.

2024-10-06 | GSE244936 | GEO

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