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Multi-omic analysis unveils biological pathways in peripheral immune system associated to minimal hepatic encephalopathy appearance in cirrhotic patients

ABSTRACT: Multi-omic analysis unveils biological pathways in peripheral immune system associated to minimal hepatic encephalopathy appearance in cirrhotic patients

PROVIDER: PRJNA629828 | ENA |

REPOSITORIES: ENA

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Multi-omic analysis unveils biological pathways in peripheral immune system associated to minimal hepatic encephalopathy appearance in cirrhotic patients

Project description:Patients with liver cirrhosis may develop minimal hepatic encephalopathy (MHE) which affects their quality of life and life span. It has been proposed that a shift in peripheral inflammation triggers the appearance of MHE. However, the mechanisms involved in this immune system shift remain unknown. In this work we studied the broad molecular changes involved in the induction of MHE with the goal of identifying (1) altered genes and pathways in peripheral blood cells associated to the appearance of MHE, (2) serum metabolites and cytokines with modified levels in MHE patients and (3) MHE-regulated immune response processes related to changes in specific serum molecules. We adopted a multi-omic approach to profile the transcriptome, metabolome and a panel of cytokines of blood samples taken from cirrhotic patients with or without MHE.

2021-01-27 | GSE149741 | GEO

Multi-omic analysis unveils biological pathways in peripheral immune system associated to minimal hepatic encephalopathy appearance in cirrhotic patients.

Project description: Not available

| S-EPMC7820002 | biostudies-literature

RNA-seq analysis of brain tissue treated by VEGFC in BDL-induced cirrhotic rat with hepatic encephalopathy

Project description:Aims: Hepatic encephalopathy (HE) is a serious neurological complication in patients with liver cirrhosis. Nothing is known about the role of the meningeal lymphatic system in HE. We tested our hypothesis that enhancement of meningeal lymphatic drainage could decrease neuroinflammation and ameliorate HE. Methods: A 4-week bile duct ligation (BDL) model was used to develop cirrhosis with HE in rats. Brain inflammation in patients with HE was evaluated using archived GSE41919. Motor function of rats was assessed by the rotarod test. AAV8-VEGF-C was injected into the cisterna magna of BDL rats one day after surgery to induce meningeal lymphangiogenesis. Results: Cirrhotic rats with HE showed significantly increased microglia activation in the middle region of the cortex (p<0.001) as well as increased neuroinflammation as indicated by significant increases in IL-1, INF, TNF and Iba1 expression in at least one of the three regions of the cortex. Motor function was also impaired in rats with HE (p<0.05). Human brains of cirrhotic patients with HE also exhibited upregulation of pro-inflammatory genes (NF-κβ, Iba1, TNFα and IL-1β) (n=6). AAV8-VEGF-C injection significantly increased meningeal lymphangiogenesis (p=0.035) and tracer dye uptake in the anterior and middle regions of the cortex (p=0.006 & 0.003, respectively), their corresponding meninges (p=0.086 & 0.006, respectively) and the draining lymph nodes (p=0.02). Further, AAV8-VEGF-C decreased microglia activation (p<0.001) and neuroinflammation, and ameliorated motor dysfunction (p=0.024). Conclusion: Promoting meningeal lymphatic drainage and enhancing waste clearance improves HE. Manipulation of meningeal lymphangiogenesis could be a new therapeutic strategy for the treatment of HE.

2023-04-23 | GSE149227 | GEO

Reversibility of minimal hepatic encephalopathy following liver transplantation in Egyptian cirrhotic patients.

Project description: Not available

| S-EPMC5084057 | biostudies-literature

Gene expression profiling in the cerebral cortex of patients with cirrhosis with and without hepatic encephalopathy

Project description:Hepatic encephalopathy (HE) is a frequent complication of liver cirrhosis and is seen as the clinical manifestation of a low grade cerebral edema associated with oxidative-nitrosative stress, however, comprehensive data on HE-associated molecular derangements in human brain are lacking. In the present study we used a whole human genome micro-array approach for gene expression profiling in post mortem brain samples from cirrhotic patients with or without HE and non-cirrhotic controls. Altered expression levels were found for a total of 1012 genes in liver cirrhotic patients without and with HE and HE-characteristic gene expression changes were identified. Genes with altered expression pattern in HE were related oxidative stress, microglia activation, inflammatory signalling pathways, cellular proliferation and apoptosis. Despite an up-regulation of genes associated with microglia activation, pro-inflammatory cytokine mRNA profiles remained unchanged in the brain of patients with liver cirrhosis and HE as compared to controls. Interestingly, many genes counteracting pro-inflammatory signalling and inflammatory cytokine expression were up-regulated in the cerebral cortex of patients with liver cirrhosis and HE. It is concluded that pathogenetic mechanisms of HE deduced from cell culture and animal experiments, such as oxidative stress, altered Zn2+-homeostasis and microglia activation also apply to human brain from cirrhotic patients with HE. The study also revealed a not yet recognized increased expression of genes antagonizing pro-inflammatory signalling and inflammatory cytokine expression. The dataset comprises 19 samples divided into three sample groups each representing a certain liver disease condition of humans.

2013-05-01 | E-GEOD-41919 | biostudies-arrayexpress

Identification of the proteins secreted by normal and cirrhotic LSECs

Project description:Normal and cirrhotic LSECs can influence hepatic stellate cells (HSCs) differently. This project aims to determine the set of proteins secreted by LSECs from healthy and cirrhotic livers, and identify the protein(s) that promote HSC activation.

2018-11-06 | PXD009010 | Pride

Gene expression profiling in the cerebral cortex of patients with cirrhosis with and without hepatic encephalopathy

2013-05-01 | GSE41919 | GEO

RNA-seq from CD4 T lymphocytes of cirrhotic patients with cognitive impairment

Project description:Patients with liver cirrhosis may have minimal hepatic encephalopathy (MHE) with cognitive and motor impairments that reduce life quality and span. MHE onset is associated with a shift in peripheral inflammation in which CD4+ lymphocytes play a key role but the underlying mechanisms remain unclear. We aimed to identify in CD4+ lymphocytes from patients with and without MHE: (1) gene expression changes and associated biological pathways using RNA-seq; (2) alterations in miRNA levels using miRNA-seq; (3) miRNAs and transcription factors regulating key mRNAs and (4) signalling pathways contributing to the peripheral inflammation shift associated to MHE onset. Additionally, we recovered T-cell receptor (TCR) repertoires from RNA-seq dataset to understand the immune status of control patients and cirrhotic patients with or without MHE.

2022-04-01 | GSE184200 | GEO

The expression of circular RNAs in tumor tissues from three non-cirrhotic hepatocellular carcinoma patients and three cirrhotic hepatocellular carcinoma patients

Project description:Six frozen hepatocellular carcinoma (HCC) samples (three without cirrhotic and three with cirrhotic background) were selected to analyze the circRNA expression profile through circRNA-seq. A total of 20334 circRNAs were identified in these tumor tissues, which were widely distributed in all chromosomes. Differential analysis revealed that 393 were significantly dysregulated in non-cirrhotic HCC when compared with cirrhotic HCC tissues (log2(fold change) > 1 and p < 0.05). Our study undoubtedly provide a new insight in investigating the initiation of HCC.

2022-05-10 | GSE193862 | GEO

Epileptic Encephalopathy

Project description:A novel null homozygous mutation confirms CACNA2D2 as a gene mutated in epileptic encephalopathy

| PRJEB4676 | ENA