ArticleJournal of leukocyte biology2015
Metabolic danger signals, uric acid and ATP, mediate inflammatory cross-talk between hepatocytes and immune cells in alcoholic liver disease.
Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Pooled it
- Comorbidities and Inflammation: How Chronic Diseases Prime the Host Response in Sepsis.International journal of molecular sciences · 2026Review
- Regulated necrosis at the crossroads of liver inflammation and cancer development.Nature reviews. Gastroenterology & hepatology · 2026Review
- IL-1 family of cytokines in gastrointestinal and liver disorders.Nature reviews. Gastroenterology & hepatology · 2026Review
- Oxidative Stress in Liver Metabolic Dysfunction and Diseases, with a Focus on Hepatogenic Diabetes: Effect of Alcohol Consumption.Antioxidants (Basel, Switzerland) · 2025Review
- Metabolites in the extracellular tumor microenvironment and the shaping of macrophage function.Molecular cell · 2025Review
- Role of Intestinal Microbiome in Potentiating Inflammation and Predicting Outcomes in Alcohol-Associated Cirrhosis.Gastroenterology clinics of North America · 2025Review
- Life-threatening risk factors contribute to the development of diseases with the highest mortality through the induction of regulated necrotic cell death.Cell death & disease · 2025Review
- The role of Triglyceride Glucose-Waist Circumference (TyG_WC) in predicting metabolic dysfunction-associated steatotic liver disease among individuals with hyperuricemia.BMC gastroenterology · 2025Article
- From stress signals to fertility challenges: the role of damage-associated molecular patterns in male reproduction.Frontiers in immunology · 2025Review
- NLRP3 Inflammasome Activation in Liver Disorders: From Molecular Pathways to Therapeutic Strategies.Journal of inflammation research · 2025Review
- Pharmacotherapy of Liver Fibrosis and Hepatitis: Recent Advances.Pharmaceuticals (Basel, Switzerland) · 2024Review
- 3PM-guided innovation in treatments of severe alcohol-associated hepatitis utilizing fecal microbiota transplantation.The EPMA journal · 2024Article
- Endothelial Dysfunction and Liver Cirrhosis: Unraveling of a Complex Relationship.International journal of molecular sciences · 2024Review
- Pathogenesis of Alcohol-Associated Liver Disease.Clinics in liver disease · 2024Review
- Inflammasomes in chronic liver disease: Hepatic injury, fibrosis progression and systemic inflammation.Journal of hepatology · 2024Review
- Article
- Cell-to-cell and organ-to-organ crosstalk in the pathogenesis of alcohol-associated liver disease.eGastroenterology · 2024Article
- The P2YPurinergic signalling · 2024Article
- Endogenous ethanol production in health and disease.Nature reviews. Gastroenterology & hepatology · 2024Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation defines the progression of ALD from reversible to advanced stages. Translocation of bacterial LPS to the liver from the gut is necessary for alcohol-induced liver inflammation. However, it is not known whether endogenous, metabolic danger signals are required for inflammation in ALD. Uric acid and ATP, 2 major proinflammatory danger signals, were evaluated in the serum of human volunteers exposed to a single dose of ethanol or in supernatants of primary human hepatocytes exposed to ethanol. In vitro studies were used to evaluate the role of uric acid and ATP in inflammatory cross-talk between hepatocytes and immune cells. The significance of signaling downstream of uric acid and ATP in the liver was evaluated in NLRP3-deficient mice fed a Lieber-DeCarli ethanol diet. Exposure of healthy human volunteers to a single dose of ethanol resulted in increased serum levels of uric acid and ATP. In vitro, we identified hepatocytes as a significant source of these endogenous inflammatory signals. Uric acid and ATP mediated a paracrine inflammatory cross-talk between damaged hepatocytes and immune cells and significantly increased the expression of LPS-inducible cytokines, IL-1β and TNF-α, by immune cells. Deficiency of NLRP3, a ligand-sensing component of the inflammasome recognizing uric acid and ATP, prevented the development of alcohol-induced liver inflammation in mice and significantly ameliorated liver damage and steatosis. Endogenous metabolic danger signals, uric acid, and ATP are involved in inflammatory cross-talk between hepatocytes and immune cells and play a crucial role in alcohol-induced liver inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.