ArticleExperimental and molecular pathology2014
The inflammasome in alcoholic hepatitis: Its relationship with Mallory-Denk body formation.
Article in Experimental and molecular pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Modulation of Inflammation-Driven Hepatocarcinogenesis: The Hepatic Immune Microenvironment, Gut-Liver Axis, and Neuroregulation.Journal of hepatocellular carcinoma · 2026Review
- Single-cell transcriptomic analysis reveals characteristic feature of macrophage reprogramming in liver Mallory-Denk bodies pathogenesis.Journal of translational medicine · 2025Article
- NLRP3 Inflammasome Activation in Liver Disorders: From Molecular Pathways to Therapeutic Strategies.Journal of inflammation research · 2025Review
- Inflammasomes in chronic liver disease: Hepatic injury, fibrosis progression and systemic inflammation.Journal of hepatology · 2024Review
- NLRP3 Inflammasome in Acute and Chronic Liver Diseases.International journal of molecular sciences · 2024Review
- Ginsenoside Rk2, a dehydroprotopanaxadiol saponin, alleviates alcoholic liver disease via regulating NLRP3 and NLRP6 inflammasome signaling pathways in mice.Journal of pharmaceutical analysis · 2023Article
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- Review
- Article
- NAIP expression increases in a rat model of liver mass restoration.Journal of molecular histology · 2021Article
- Low Interleukin-22 Binding Protein Is Associated With High Mortality in Alcoholic Hepatitis and Modulates Interleukin-22 Receptor Expression.Clinical and translational gastroenterology · 2020Article
- Lytic cell death in metabolic liver disease.Journal of hepatology · 2020Review
- MicroRNA-141 ameliorates alcoholic hepatitis‑induced intestinal injury and intestinal endotoxemia partially via a TLR4-dependent mechanism.International journal of molecular medicine · 2019Article
- [Role of NLRP3 inflammasome in the pathogenesis of alcoholic liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2019Article
- Article
- A Unifying Hypothesis Linking Hepatic Adaptations for Ethanol Metabolism to the Proinflammatory and Profibrotic Events of Alcoholic Liver Disease.Alcoholism, clinical and experimental research · 2018Review
- New insights into Nod-like receptors (NLRs) in liver diseases.International journal of physiology, pathophysiology and pharmacology · 2018Review
- Gut-liver axis and sterile signals in the development of alcoholic liver disease.Alcohol and alcoholism (Oxford, Oxfordshire) · 2017Review
- Target acquired: Selective autophagy in cardiometabolic disease.Science signaling · 2017Review
- Role of Protein Quality Control Failure in Alcoholic Hepatitis Pathogenesis.Biomolecules · 2017Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Recent studies indicate that the inflammasome activation plays important roles in the pathogenesis of alcoholic hepatitis (AH). Nod-like receptor protein 3 (NLRP3) is a key component of the macromolecular complex that is so called the inflammasome that triggers caspase 1-dependent maturation of the precursors of IL-1β and IL-18 cytokines. It is also known that the adaptor proteins including apoptosis-associated speck-like protein containing CARD (ASC) and the mitochondrial antiviral signaling protein (MAVS) are necessary for NLRP3-dependent inflammasome function. Steatohepatitis frequently includes Mallory-Denk body (MDB) formation. In the case of alcoholic steatohepatitis, MDB formation occurs in 80% of biopsies (French 1981; French 1981). While previous studies have focused on in vitro cell lines and mouse models, we are the first group to investigate inflammasome activation in AH liver biopsy specimen and correlate it with MDB formation. Expression of NOD1, NLRP3, ASC, NAIP, MAVS, caspase 1, IL-1β, IL-18, and other inflammatory components including IL-6, IL-10, TNF-α, IFN-γ, STAT3, and p65 was measured in three to eight formalin-fixed paraffin-embedded AH specimens and control normal liver specimens by immunofluorescence staining and quantified by immunofluorescence intensity. The specimens were double stained with ubiquitin to demonstrate the relationship between inflammasome activation and MDB formation. MAVS, caspase1, IL-18, and TNF-α showed increases in expression in AH compared to the controls (p<0.05), and NAIP expression markedly increased in AH compared to the controls (p<0.01). There was a trend that levels of NLRP3, ASC, caspase1, IL-18, IL-10, and p65 expression correlated with the number of MDBs found in the same field of measurement (correlation coefficients were between 0.62 and 0.93, p<0.05). Our results demonstrate the activation of the inflammasome in AH and suggest that MDB could be an indicator of the extent of inflammasome activation.
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