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Circulating neutrophil transcriptomics in HBV-ACLF patients.

ABSTRACT: Circulating neutrophil transcriptomics in HBV-ACLF patients.

PROVIDER: PRJNA692986 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13455170_1.fastq.gz	Fastqsanger.gz
	SRR13455170_2.fastq.gz	Fastqsanger.gz
	SRR13455171_1.fastq.gz	Fastqsanger.gz
	SRR13455171_2.fastq.gz	Fastqsanger.gz
	SRR13455172_1.fastq.gz	Fastqsanger.gz

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Circulating neutrophil transcriptomics in HBV-ACLF patients.

Project description:The transcriptomic profiles of circulating neutrophils were compared between patients with ACLF (N=10), patients with CLC (N=10) and HC (N=10). Compared with CLC-neutrophils, the expression of 1022 genes were found to be upregulated in ACLF-neutrophils, and 1101 genes were downregulated. And compared to HC, the expression of 726 genes were up-regulated in ACLF-neutrophils, and 711 genes were down-regulated. The pathway analysis identified mutiple pathways enriched or down-regulated in ACLF-neutrophils when comparing with neutrophils from CLC or HC groups.

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Prognosis associated microRNA in peripheral blood mononuclear cells (PBMCs) from hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) [miRNA]

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Quantitative Proteomic Analysis of Plasma Samples from Chronic Hepatitis B and Chronic Liver Failure Patients for Biomarker Discovery

Project description:Hepatitis B virus (HBV)-associated acute on chronic liver failure (HBV-ACLF), characterized by an acute deterioration of liver function in the patients with chronic hepatitis B (CHB), is lack of predicting biomarkers for prognosis. To explore potential biomarkers of HBV-ACLF for clinical applications, immuno-depletion of high-abundance plasma proteins followed by iTRAQ-based quantitative proteomic approach was employed to analyze plasma samples from 20 healthy control people, 20 CHB patients and 20 HBV-ACLF patients, respectively. As a result, a total of 427 proteins were identified and quantified from these samples, and 42 proteins were differentially expressed in HBV-ACLF patients as compared to both CHB patients and healthy controls. According to bioinformatics analysis results, 6 proteins related to immune response (MMR), inflammatory response (OPN, HPX), blood coagulation (ATIII) and lipid metabolism (APO-CII, GP73) were selected as biomarker candidates. Further ELISA analysis confirmed the significant up-regulation of GP73, MMR, OPN and down-regulation of ATIII, HPX, APO-CII in HBV-ACLF plasma samples (p<0.01). Moreover, receiver operating characteristic (ROC) curve analysis revealed high diagnostic value of these candidates in assessing HBV-ACLF. In conclusion, present quantitative proteomic study identified 6 novel HBV-ACLF biomarker candidates and might provide fundamental information for development of HBV-ACLF biomarker.

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Project description:To address the molecular basis of immune-dysfunction in Acute-on-chronic liver failure (ACLF), we carried out gene expression profiling of blood derived neutrophil from ACLF, belonging to both sterile inflammatory and sepsis conditions. Peripheral whole blood was subjected to PMN enrichment by double gradient centrifugation, and RNA isolation was done by TRIZOL method, followed by microarray experiment using Agilent one-color platform. We compared the gene expression of these neutrophils with that of Chronic liver disease (CLD) patients and healthy controls (HC) for baseline relative quantification, and found unique set of upregulated and downregulated genes in ACLF. We validated the expression of the most differentially expressed genes by quantitative RT-PCR and also stratified the patients into survivors and non-survivors, sepsis and sterile-inflammation. We found an upregulated 3-gene signature of ELANE-MPO-CD177 to be associated with 28-day mortality, irrespective of presence or absence of sepsis.

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Sepsis related ACLF mouse model

Project description:Background and aims: Acute-on-chronic liver failure (ACLF) is an acute liver and multisystem failure in patients with previously stable cirrhosis. A common cause of ACLF is sepsis secondary to bacterial infection. Sepsis-associated ACLF involves a loss of differentiated liver function in the absence of direct liver injury, and its mechanism is unknown. We aimed to study the mechanism of sepsis associated ACLF using a novel mouse model. Approach and Results: Sepsis-associated ACLF was induced by cecal ligation and puncture procedure (CLP) in mice treated with thioacetamide (TAA). The combination of TAA and CLP resulted in a significant decrease in liver synthetic function and high mortality. These changes were associated with reduced metabolic gene expression and increased C/EBPβ transcriptional activity. We found that C/EBPβ binding to its target gene promoters was increased. In humans C/EBPβ chromatin binding was similarly increased in ACLF group compared to control cirrhosis. Hepatocyte specific Cebpb knockout mice had reduced mortality and increased gene expression of hepatocyte differentiation markers in TAA/CLP mice, suggesting that C/EBPβ promotes liver failure in these mice. C/EBPβ activation was associated with endothelial dysfunction, characterized by reduced Angiopoietin-1/Angiopoietin-2 ratio and increased endothelial production of HGF. Angiopoietin-1 supplementation or Hgf knockdown reduced hepatocyte C/EBPβ accumulation, restored liver function, and reduced mortality, suggesting that endothelial dysfunction induced by sepsis drives acute-on-chronic liver failure via HGF-C/EBPβ pathway. Conclusion: The transcription factor C/EBPβ is activated in both mouse and human ACLF and is a potential therapeutic target to prevent liver failure in patients with sepsis and cirrhosis.

2023-04-04 | GSE228610 | GEO

Comparative proteomics analysis of serum protein factors for predicting the prognosis of HBV-related acute-on-chronic liver failure (ACLF)

Project description:Acute-on-chronic liver failure (ACLF) is an acute deterioration of liver function in patients with hepatitis B virus-related cirrhosis. Numerous risk factors were determined to predict the mortality of HBV-related ACLF. However, little is known about the whole serum proteome profiles in ACLF patients. Here, we perform a comparative proteomics analysis to describe the difference of the proteome profiles between the serum samples from survival (S) and death (D) ACLF patients on the day of hospitalization (H) and after four weeks (F) of treatment in hospital. A total of 518 proteins were identified, of which 295 were considered as high-quality proteins (95% peptides ≥ 2). Together, 112 proteins showed significantly different abundant (DAPs). The GO enrichment analysis showed that the DAPs between S and D group at the day of hospitalization were mostly located in lipoprotein particles and synaptic vesicle. Notably, six proteins showed continuously different abundant between S and D groups, both at H and F time point. We further validated three protein factors for predicting the prognosis of ACLF by ELISA in expanded samples, resulting in a 92.22% AUC for combination of ITIH3 and APO-C1 proteins. These proteins may serve as novel factors for predicting the prognosis of HBV-related ACLF. This study provided an overview of proteome profiles between survived and dead ACLF patients and reveals novel serum factors for predicting the prognosis of this extreme condition.

2019-04-19 | PXD013582 |

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