ArticleHepatology (Baltimore, Md.)2020
Paneth Cell Dysfunction Mediates Alcohol-related Steatohepatitis Through Promoting Bacterial Translocation in Mice: Role of Zinc Deficiency.
Article in Hepatology (Baltimore, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 3 of them syntheses that pooled it.
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Who cites it
57 citing papers in PubMed, 3 syntheses or guidelines pooled it, 67 citations in OpenAlex.
- Analysis of Antimicrobial Peptide Expression Under Acute and Chronic Alcohol Exposure: A Cross-Sectional Study and a Systematic Review of the Literature.International journal of molecular sciences · 2026Pooled it
- Influence of Alcohol on the Intestinal Immune System.Alcohol research : current reviews · 2025Pooled it
- Paneth Cells: Recent Updates on Elucidating Therapeutic Implications in Gastroenterological Disease Management.Current medicinal chemistry · 2025Pooled it
- Inflammatory gut-liver crosstalk: mechanisms and therapeutic targets.Experimental & molecular medicine · 2026Review
- Gut-liver axis molecular mechanisms in alcohol-associated liver disease.Alcohol (Fayetteville, N.Y.) · 2026Review
- Bifidobacterium bifidum-derived nanoparticles attenuate alcoholic liver disease via enhanced hepatic phagocytosis and gastrointestinal homeostasis.Nature communications · 2026Article
- Jejunum and ileum histopathology in male Sprague-Dawley rats exposed to alcohol and combination anti-retroviral therapy.Anatomy & cell biology · 2026Article
- Paneth cells as orchestrators of epithelial barrier defense and emerging therapeutic targets in inflammatory bowel disease.Seminars in immunopathology · 2026Review
- Antimicrobial proteins and peptides in pregnancy: Guardians of the maternal-fetal frontier.Frontiers in immunology · 2026Review
- Transition From a High-Sugar and Butter to a Standard Diet Leads to Cecal Dysbiosis, Disrupts Intestinal Homeostasis, and Favors Increased Ethanol Consumption and Preference.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- New mouse model based on adenocarcinoma 4T1 cells expressing HPV16 E6 and E7 applied to assess the efficacy of therapeutic and prophylactic E6/E7-based HPV16 vaccines.Infectious agents and cancer · 2025Article
- Macrophage Signaling Pathways in Health and Disease: From Bench to Bedside Applications.MedComm · 2025Review
- Hepatic NMNAT1 is required to defend against alcohol-associated fatty liver disease.Science advances · 2025Article
- Malnutrition in Substance Use Disorders: A Critical Issue in Their Treatment and Recovery.Healthcare (Basel, Switzerland) · 2025Review
- Gut microbiota in the development and progression of chronic liver diseases: Gut microbiota-liver axis.World journal of hepatology · 2025Review
- Gut microbiome and liver diseases.Fundamental research · 2025Review
- Excessive alcohol consumption: a driver of metabolic dysfunction and inflammation.Frontiers in toxicology · 2025Review
- Gut Microbiota as Emerging Players in the Development of Alcohol-Related Liver Disease.Biomedicines · 2024Review
- NLRP3 activation maintains intestinal epithelial barrier and reduces liver injury in alcoholic liver disease mice.Clinical and translational medicine · 2024Article
- Gut-liver axis: Recent concepts in pathophysiology in alcohol-associated liver disease.Hepatology (Baltimore, Md.) · 2024Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsMicrobial dysbiosis is associated with alcohol-related hepatitis (AH), with the mechanisms yet to be elucidated. The present study aimed to determine the effects of alcohol and zinc deficiency on Paneth cell (PC) antimicrobial peptides, α-defensins, and to define the link between PC dysfunction and AH. APPROACH AND
resultsTranslocation of pathogen-associated molecular patterns (PAMPs) was determined in patients with severe AH and in a mouse model of alcoholic steatohepatitis. Microbial composition and PC function were examined in mice. The link between α-defensin dysfunction and AH was investigated in α-defensin-deficient mice. Synthetic human α-defensin 5 (HD5) was orally given to alcohol-fed mice to test the therapeutic potential. The role of zinc deficiency in α-defensin was evaluated in acute and chronic mouse models of zinc deprivation. Hepatic inflammation was associated with PAMP translocation and lipocalin-2 (LCN2) and chemokine (C-X-C motif) ligand 1 (CXCL1) elevation in patients with AH. Antibiotic treatment, lipopolysaccharide injection to mice, and in vitro experiments showed that PAMPs, but not alcohol, directly induced LCN2 and CXCL1. Chronic alcohol feeding caused systemic dysbiosis and PC α-defensin reduction in mice. Knockout of functional α-defensins synergistically affected alcohol-perturbed bacterial composition and the gut barrier and exaggerated PAMP translocation and liver damage. Administration of HD5 effectively altered cecal microbial composition, especially increased Akkermansia muciniphila, and reversed the alcohol-induced deleterious effects. Zinc-regulated PC homeostasis and α-defensins function at multiple levels, and dietary zinc deficiency exaggerated the deleterious effect of alcohol on PC bactericidal activity.
conclusionsTaken together, the study suggests that alcohol-induced PC α-defensin dysfunction is mediated by zinc deficiency and involved in the pathogenesis of AH. HD5 administration may represent a promising therapeutic approach for treating AH.
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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.