ArticleJournal of leukocyte biology2006
Chronic ethanol feeding increases activation of NADPH oxidase by lipopolysaccharide in rat Kupffer cells: role of increased reactive oxygen in LPS-stimulated ERK1/2 activation and TNF-alpha production.
Article in Journal of leukocyte biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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Who cites it
118 citing papers in PubMed, 196 citations in OpenAlex.
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- Toll/IL-1 receptor domain-containing adaptor protein plays a crucial role in macrophage-mediated hepatic stellate cell activation in alcoholic liver disease.Frontiers in cell and developmental biology · 2026Article
- Methionine Adenosyltransferase 1A and S-Adenosylmethionine in Alcohol-Associated Liver Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Myeloid cells in chronic liver inflammation.Cellular & molecular immunology · 2025Review
- Liver immunology: Biological role and clinical significance.World journal of hepatology · 2025Review
- Binge drinking triggers VGLUT3-mediated glutamate secretion and subsequent hepatic inflammation by activating mGluR5/NOX2 in Kupffer cells.Nature communications · 2025Article
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- Reactive Oxygen Species as a Common Pathological Link Between Alcohol Use Disorder and Alzheimer's Disease with Therapeutic Implications.International journal of molecular sciences · 2025Review
- Nicotinamide Adenine Dinucleotide Phosphate Oxidases and Metabolic Dysfunction-Associated Steatotic Liver Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Insights of gut-liver axis in hepatic diseases: Mechanisms, clinical implications, and therapeutic potentials.World journal of gastrointestinal pharmacology and therapeutics · 2024Review
- Cell-to-cell and organ-to-organ crosstalk in the pathogenesis of alcohol-associated liver disease.eGastroenterology · 2024Article
- Systemic low-dose anti-fibrotic treatment attenuates ovarian aging in the mouse.bioRxiv : the preprint server for biology · 2024Article
- The Role of Cytokines in the Pathogenesis and Treatment of Alcoholic Liver Disease.Diseases (Basel, Switzerland) · 2024Review
- Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption.Antioxidants (Basel, Switzerland) · 2023Review
- The Intestinal Microbiota in the Development of Chronic Liver Disease: Current Status.Diagnostics (Basel, Switzerland) · 2023Review
- Thioredoxin/Glutaredoxin Systems and Gut Microbiota in NAFLD: Interplay, Mechanism, and Therapeutical Potential.Antioxidants (Basel, Switzerland) · 2023Review
- Autophagy, Oxidative Stress, and Alcoholic Liver Disease: A Systematic Review and Potential Clinical Applications.Antioxidants (Basel, Switzerland) · 2023Review
- Bioactive Compounds as Inhibitors of Inflammation, Oxidative Stress and Metabolic Dysfunctions via Regulation of Cellular Redox Balance and Histone Acetylation State.Foods (Basel, Switzerland) · 2023Review
- Probiotics-FermentedInternational journal of molecular sciences · 2023Article
58 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) contribute to the development of chronic ethanol-induced liver injury. Although ROS modulate the activity of many signal transduction pathways, the molecular targets of ROS during ethanol exposure are not well understood. Here, we investigated whether specific ROS-sensitive signal transduction pathways contribute to increased tumor necrosis factor alpha (TNF-alpha) production by Kupffer cells after chronic ethanol feeding to rats. Lipopolysaccharide (LPS) rapidly increased ROS production, measured by dihydrorhodamine fluorescence, in Kupffer cells from ethanol- and pair-fed rats, and ROS production was 2.5-fold greater in ethanol-fed compared with pair-fed. Pretreatment with diphenyleneiodonium (DPI), which inhibits reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, normalized ROS production in Kupffer cells from ethanol-fed rats. LPS rapidly increased Rac1-guanosinetriphosphatase (GTPase) activity and p67(phox) translocation to the plasma membrane in Kupffer cells from pair-fed rats. After ethanol feeding, Rac1-GTPase activity was already increased over pair-fed at baseline and remained elevated over pair-fed after LPS stimulation. Further, LPS-stimulated p67(phox) translocation to the plasma membrane was enhanced after chronic ethanol feeding. LPS-stimulated extracellular signal-regulated kinase (ERK)1/2 and p38 phosphorylation, two signaling pathways regulated by ROS, were increased twofold in Kupffer cells from ethanol-fed rats compared with pair-fed controls. However, only LPS-stimulated ERK1/2 phosphorylation was inhibited by DPI, which also reduced LPS-stimulated TNF-alpha production in Kupffer cells from pair- and ethanol-fed rats. These results demonstrate that chronic ethanol feeding increases LPS-stimulated NADPH oxidase-dependent production of ROS in Kupffer cells. Further, ERK1/2 is an important target of NADPH oxidase-derived ROS in Kupffer cells, contributing to enhanced LPS-stimulated TNF-alpha production by Kupffer cells after chronic ethanol feeding.
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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.