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    Home > Active Ingredient News > Digestive System Information > Gut Zhejiang University Li Jun/Chen Xin/Wang Di reveal the molecular basis of hepatitis B virus-related acute and chronic liver failure

    Gut Zhejiang University Li Jun/Chen Xin/Wang Di reveal the molecular basis of hepatitis B virus-related acute and chronic liver failure

    • Last Update: 2021-11-04
    • Source: Internet
    • Author: User
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    Editor’s note iNature is China’s largest academic official account.
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    In iNature, patients with chronic liver disease will suffer from acute-chronic liver failure (ACLF) regardless of whether there is cirrhosis of the liver, and it is a common final route leading to death
    .

    Understanding the molecular mechanism of ACLF is essential to develop effective early diagnosis and treatment strategies
    .

    The pathophysiology of hepatitis B virus-related acute chronic liver failure (HBV-ACLF) is still unclear
    .

    This study aims to use transcriptomics to characterize the molecular basis of HBV-ACLF
    .

    On October 18, 2021, Li Jun, Chen Xin, Wang Di of Zhejiang University, and Jonel Trebicka of Frankfurt University, Germany, published an online newsletter titled "PBMC transcriptomics identifies immune-metabolism disorder during the development of HBV-" on Gut (IF=23.
    06).
    ACLF" research paper, the study of 400 HBV-ACLF, acute chronic liver dysfunction (ACHD), liver cirrhosis (LC) or chronic hepatitis B (CHB) and normal controls (NC) from a prospective multicenter cohort Of subjects were studied, 65 subjects (ACLF, 20; ACHD, 10; LC, 10; CHB, 10; NC, 15) received mRNA sequencing using peripheral blood mononuclear cells (PBMC)
    .

    A functional synergy analysis of seven biological processes related to PBMC response and the first 500 differentially expressed genes (DEG) showed that viral processes are related to all disease stages
    .

    Immune disorders are the most significant changes and disorders caused by the deterioration of HBV, which promotes the development of CHB or LC into ACHD and ACLF
    .

    Metabolic disorders are significant in ACHD and severe in ACLF
    .

    The analysis of 62 overlapping DEGs further linked HBV-based immune metabolic disorders to ACLF progress
    .

    The characteristics of interferon-related, neutrophil-related and monocyte-related pathways related to the innate immune response were significantly up-regulated; the characteristics related to the adaptive immune response were down-regulated
    .

    Disruption of lipid and fatty acid metabolism was observed during the development of ACLF
    .

    The external verification of the four DEGs behind the above-mentioned molecular mechanisms in patients and experimental rats confirmed their specificity and potential as biomarkers for the pathogenesis of HBV-ACLF
    .

    In conclusion, the study emphasizes that the immune metabolic disorder caused by the deterioration of HBV is a potential mechanism of HBV-ACLF, and may provide a new diagnostic and therapeutic target for reducing HBV-ACLF-related mortality
    .

    Acute-chronic liver failure (ACLF) occurs in patients with chronic liver disease regardless of the presence of cirrhosis, and it is a common final route leading to death
    .

    Understanding the molecular mechanism of ACLF is essential to develop effective early diagnosis and treatment strategies
    .

    The Chronic Liver Failure (CLIF) Alliance Acute Liver Cirrhosis and Chronic Liver Failure (CANONIC) study first developed the ACLF definition and diagnostic criteria for patients with acute decompensated alcoholic liver disease or hepatitis C virus-related cirrhosis
    .

    The accepted definition recognizes ACLF as a unique syndrome based on organ failure and high mortality
    .

    A recent large-scale prospective multi-center study (China Severe Hepatitis B Research Group, COSSH) documented that hepatitis B virus-related ACLF (HBV-ACLF) showed clinical features different from ACLF related to alcoholic liver disease in Western populations.
    The COSSH-ACLF criteria for ACLF diagnosis in HBV-positive populations are proposed because these criteria show higher diagnostic sensitivity and prognostic accuracy
    .

    It is known that liver cell damage and death can trigger ACLF; however, the cause of liver cell damage and the pathways involved in the progression of ACLF are still unclear
    .

    CANONIC research shows that strong systemic inflammatory response is the main reason for the acute exacerbation of patients with alcoholic liver disease-related and hepatitis C virus-related ACLF
    .

    As mentioned earlier, the two largest ACLF prospective multi-center studies to date, CANONIC and COSSH, revealed the regional phenotypic differences in ACLF disease etiology and precipitating events
    .

    In this study, the aim is to provide a transcriptomics-based data set derived from circulating immune cells (peripheral blood mononuclear cells, PBMC) collected at different stages of disease progression in HBV-ACLF patients to clarify disease development The detailed molecular mechanism of HBV-ACLF and the effects of liver tissue and prognosis in patients with HBV-ACLF, as well as the development and validation of potential biomarkers to improve the diagnosis and prognosis of HBV-ACLF
    .

    The study was conducted on 400 subjects with HBV-ACLF, acute chronic liver dysfunction (ACHD), liver cirrhosis (LC) or chronic hepatitis B (CHB) and normal controls (NC) from a prospective multicenter cohort In the study, 65 subjects (ACLF, 20; ACHD, 10; LC, 10; CHB, 10; NC, 15) received mRNA sequencing using peripheral blood mononuclear cells (PBMC)
    .

    A functional synergy analysis of seven biological processes related to PBMC response and the first 500 differentially expressed genes (DEG) showed that viral processes are related to all disease stages
    .

    Immune disorders are the most significant changes and disorders caused by the deterioration of HBV, which promotes the development of CHB or LC into ACHD and ACLF
    .

    Metabolic disorders are significant in ACHD and severe in ACLF
    .

    The analysis of 62 overlapping DEGs further linked HBV-based immune metabolic disorders to ACLF progress
    .

    The characteristics of interferon-related, neutrophil-related and monocyte-related pathways related to the innate immune response were significantly up-regulated; the characteristics related to the adaptive immune response were down-regulated
    .

    Disruption of lipid and fatty acid metabolism was observed during the development of ACLF
    .

    The external verification of the four DEGs behind the above-mentioned molecular mechanisms in patients and experimental rats confirmed their specificity and potential as biomarkers for the pathogenesis of HBV-ACLF
    .

    In conclusion, this study emphasizes that the immune metabolic disorder caused by the deterioration of HBV is a potential mechanism of HBV-ACLF, and may provide a new diagnostic and therapeutic target for reducing HBV-ACLF-related mortality
    .

    Reference message: https://gut.
    bmj.
    com/content/early/2021/10/18/gutjnl-2020-323395
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