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Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis [bulk RNASeq]

ABSTRACT: Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis [bulk RNASeq]

PROVIDER: PRJNA961704 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24300900.fastq.gz	Fastqsanger.gz
	SRR24301000.fastq.gz	Fastqsanger.gz
	SRR24300901.fastq.gz	Fastqsanger.gz
	SRR24301001.fastq.gz	Fastqsanger.gz
	SRR24300902.fastq.gz	Fastqsanger.gz

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Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis [scData]

Project description:Primary sclerosing cholangitis (PSC) is an autoimmune-like disease of the bile ducts that co-occurs with inflammatory bowel disease (IBD) in almost 90% of cases. Colorectal cancer is a major complication of patients with both PSC and IBD, and these patients are at a much greater risk compared to patients with IBD without concomitant PSC. Combining flow cytometry, bulk and single cell transcriptomics, and T- and B-cell receptor repertoire analysis of right colon tissue from PSC, IBD, and healthy controls we identified a unique adaptive inflammatory transcriptional signature associated with greater risk and shorter time to dysplasia specifically in patients with PSC. This inflammatory signature is characterized by antigen-driven IL-17A+ Foxp3+ CD4 T-cell and an expansion of IgG-secreting B-cell responses. These data results suggest that the mechanisms that drive the emergence of dysplasia in of PSC and IBD dysplasia are distinct and provide molecular insights to guide prevention of colorectal cancer in PSC.

2023-04-30 | GSE230568 | GEO

Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis

Project description:Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis

| PRJNA961773 | ENA

Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis [bulk RNASeq]

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Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis [scData]

Project description:Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis [scData]

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Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis.

Project description:Primary sclerosing cholangitis (PSC) is an immune-mediated disease of the bile ducts that co-occurs with inflammatory bowel disease (IBD) in almost 90% of cases. Colorectal cancer is a major complication of patients with PSC and IBD, and these patients are at a much greater risk compared to patients with IBD without concomitant PSC. Combining flow cytometry, bulk and single-cell transcriptomics, and T and B cell receptor repertoire analysis of right colon tissue from 65 patients with PSC, 108 patients with IBD and 48 healthy individuals we identified a unique adaptive inflammatory transcriptional signature associated with greater risk and shorter time to dysplasia in patients with PSC. This inflammatory signature is characterized by antigen-driven interleukin-17A (IL-17A)+ forkhead box P3 (FOXP3)+ CD4 T cells that express a pathogenic IL-17 signature, as well as an expansion of IgG-secreting plasma cells. These results suggest that the mechanisms that drive the emergence of dysplasia in PSC and IBD are distinct and provide molecular insights that could guide prevention of colorectal cancer in individuals with PSC.

| S-EPMC10287559 | biostudies-literature

Serum and bile proteomics reveal candidates for new noninvasive serum markers of primary sclerosing cholangitis and of risk of disease progression and biliary neoplasia.

Project description:Primary sclerosing cholangitis (PSC) is a chronic liver disease characterized by biliary strictures, cholestasis, and an increased risk of cholangiocarcinoma (CCA). Here, we have used label-free quantitative proteomics to analyze serum and bile samples from non-PSC controls and PSC patients, as well as from PSC patients divided into groups according to endoscopic retrograde cholangiography score (with a score of >4 indicating advanced disease) and presence or absence of biliary dysplasia/CCA. Further analyses subsequently identified multiple candidates of new noninvasive serum markers for the diagnosis of PSC, as well as new markers for the prediction of the risk of disease progression and biliary neoplasia for patients already diagnosed with PSC.

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Serum and bile proteomics reveal candidates for new noninvasive serum markers of primary sclerosing cholangitis and of risk of disease progression and biliary neoplasia (BILE)

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STAT3 protects from liver injury and fibrosis in a mouse model of sclerosing cholangitis

Project description:Background and aims: Signal transducer and activator of transcription 3 (Stat3) is the main mediator of interleukin-6 type cytokine signaling required for hepatocyte proliferation and hepatoprotection but its role in sclerosing cholangitis and other cholestatic liver diseases remains unresolved. Methods: We investigated the role of Stat3 in inflammation-induced cholestatic liver injury and used mice lacking the multidrug resistance gene 2 (mdr2-/-) as a model for SC. Results: We demonstrate that conditional inactivation of stat3 in hepatocytes and cholangiocytes (stat3 delta hc) of mdr2-/- mice strongly aggravated bile acid-induced liver injury and fibrosis. A similar phenotype was observed in mdr2-/- mice lacking IL-6 production. Biochemical and molecular characterization suggested that Stat3 exerts hepatoprotective functions in both, hepatocytes and cholangiocytes. Loss of Stat3 in cholangiocytes led to increased expression of TNFÎ± which might reduce the barrier function of bile ducts. Loss of Stat3 in hepatocytes led to upregulation of bile acid biosynthesis genes and downregulation of hepatoprotective epidermal growth factor receptor and insulin-like growth factor 1 signaling pathways. Consistently, stat3deltahc mice were more sensitive to cholic acid-induced liver damage than control mice. Conclusions: Our data suggest that Stat3 prevents cholestasis and liver damage in sclerosing cholangitis via regulation of pivotal functions in hepatocytes and cholangiocytes. Affymetrix microarray analyses was performed to identify metabolic and molecular pathways in stat3Dhc mdr2-/- mice that lead to cholestasis and bile acid-induced liver injury. To avoid false positive results that are due to differential cellular composition, we defined the onset of fibrosis and expression of fibrogenic factors in stat3Dhc mdr2-/- mice.

2010-10-20 | E-GEOD-18759 | biostudies-arrayexpress

Downregulation of TGR5 (GPBAR1) in biliary epithelial cells is characteristic of sclerosing cholangitis and may contribute to disease pathogenesis

Project description:Primary sclerosing cholangitis (PSC) is characterized by chronic inflammation and progressive fibrosis of the biliary tree. The bile acid receptor TGR5 is found on biliary epithelial cells (BECs), where it promotes secretion, proliferation and tight junction integrity. Thus, we speculated that changes in TGR5 expression in BECs may contribute to PSC pathogenesis.

2021-03-12 | GSE168758 | GEO

Compare Conventional Colonosocpy to Endoscopic AFI, NBI for Dysplasia Detection for Ulcerative Colitis & Cholangitis

Project description:This study is being done to: To attempt to increase the detection of precancerous colon tissue in patients with chronic ulcerative colitis and primary sclerosing cholangitis; To determine if an investigational scope that can look at the lining of the colon in different ways will help the doctor identify abnormal tissue in patients with chronic ulcerative colitis and concurrent primary sclerosing cholangitis; and To determine if this investigational scope can accurately detect precancerous or cancerous tissue in patients with chronic ulcerative colitis that are known to have had cancerous or precancerous tissue in the past.

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