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Human gut metagenome

ABSTRACT: Investigation of the microbiota in bile duct of primary sclerosing cholangitis and cholestasis.

PROVIDER: PRJDB18053 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR550145_1.fastq.gz	Fastqsanger.gz
	DRR550145_2.fastq.gz	Fastqsanger.gz
	DRR550146_1.fastq.gz	Fastqsanger.gz
	DRR550146_2.fastq.gz	Fastqsanger.gz
	DRR550147_1.fastq.gz	Fastqsanger.gz

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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.

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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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Project description:Cholangiopathies such as Primary Sclerosing Cholangitis (PSC) cause damage to the bile ducts and fibrosis with no effective cure. A reduction and impairment in the function of regulatory T cells (Tregs) occur in PSC. Yet, it is currently unknown what consequence this has on bile duct regeneration. We investigate whether Tregs regulate bile duct regeneration and the dynamics of Tregs turnover during bile duct injury. We used the transgenic Foxp3GFPDTR model to mimic reduced Tregs infiltration to the liver during bile duct injury and showed that reduced intrahepatic Tregs limits bile duct regeneration. Fate mapping of Tregs (Foxp3CreERTAi14) showed that Tregs acquire a pro-inflammatory phenotype within the inflammatory microenvironment, even after IL2 mediated Tregs expansion. Ox40L expression correlates with fibrosis in PSC patients. In the 3,5-Diethoxycarbonyl-1,4-Dihydrocollidine (DDC)-diet mouse model of experimental cholangiopathy, combining IL2-complex administration and blocking Ox40L decreases periportal fibrosis level, increases Treg number and reduces the pro-inflammatory phenotype of Tregs. These results indicate that Tregs mediate cholangiocyte response to biliary injury, and Tregs downregulate Foxp3 and acquire an inflammatory phenotype in an inflammatory microenvironment. Enhancing Treg numbers through IL2 complex administration and blocking Ox40 signalling simultaneously suppress the inflammatory phenotype of Tregs and reduce bile duct damage and fibrosis.

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2021-03-12 | GSE168758 | GEO

Primary sclerosing cholangitis-specific inflammatory bowel disease phenotype is driven by an altered immune system shaped by circulatory markers.

Project description:Approximately 80% of patients with Primary Sclerosing Cholangitis (PSC) also have an underlying Inflammatory Bowel Disease (IBD). Notably, PSC-IBD presents a unique phenotype compared to Ulcerative Colitis or Crohn’s Disease alone , which may increase the risk of colitis-associated neoplasia. This case-control study comprises a cohort of 15 patients in the PSC-IBD group, 30 patients in the IBD-alone group, and 19 patients in the control group. Through the analysis of patient serum and colon tissue proteomics, colon gene expression, fecal gut microbiota, and in vitro data with human monocytes, we identified a specific interplay between systemic circulation and gut microbiota dysbiosis that may predispose PSC-IBD patients to neoplasia development. Our study revealed that PSC-IBD patients show a shift in gut microbiota towards an increase in Intestinibacter, a bacterium known to exacerbate IBD conditions.Interestingly, when comparing the PSC-IBD group to the IBD-alone group, we observed elevated miR-21 expression levels in fasting serum and stool samples. Finally, we partially reproduce the inflammatory PSC-IBD profile using miR-21 and bile acid GCDCA stimulus in human-derived monocytes. Our findings suggest that circulating miR-21, along with bile acid GCDCA, tissue macrophage recruitment, and distinct microbiota profiles, may contribute to the unique phenotype of IBD in PSC patients.

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