ArticleInternational journal of molecular sciences2019
Exogenous Administration of Low-Dose Lipopolysaccharide Potentiates Liver Fibrosis in a Choline-Deficient l-Amino-Acid-Defined Diet-Induced Murine Steatohepatitis Model.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- The Efficacy of Gut Microbiome-Modulating Therapies on Liver Cirrhosis: A Systematic Review and Network Meta-Analysis.Clinical and translational gastroenterology · 2026Pooled it
- Titanium dioxide nanoparticles: revealing the mechanisms underlying hepatotoxicity and effects in the gut microbiota.Archives of toxicology · 2023Pooled it
- Bifidobacterium breve BBr60 Improves Metabolic Abnormalities by Regulating Gut Microbiota Balance in a High-Fat Diet-Induced Obese Mouse Model.Diabetes, obesity & metabolism · 2026Article
- The Dual Role of Gut Microbiota and Their Metabolites in Hepatocellular Carcinoma: A Context-Dependent Framework.Microorganisms · 2025Review
- Effect ofFEMS microbes · 2025Article
- Dietary Influences on Gut Microbiota and Their Role in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Nutrients · 2024Review
- Ginger essential oil prevents NASH progression by blocking the NLRP3 inflammasome and remodeling the gut microbiota-LPS-TLR4 pathway in mice.Nutrition & diabetes · 2024Article
- Article
- Body Composition in Chronic Liver Disease.International journal of molecular sciences · 2024Review
- Healthy diet intervention reverses the progression of NASH through gut microbiota modulation.Microbiology spectrum · 2024Article
- An update on animal models of liver fibrosis.Frontiers in medicine · 2023Review
- Host-microbiome interactions: Gut-Liver axis and its connection with other organs.NPJ biofilms and microbiomes · 2022Review
- Induction of Accelerated Aging in a Mouse Model.Cells · 2022Review
- Colesevelam ameliorates non-alcoholic steatohepatitis and obesity in mice.Hepatology international · 2022Article
- Traditional Chinese medicine: An important source for discovering candidate agents against hepatic fibrosis.Frontiers in pharmacology · 2022Review
- Local free fatty acids trigger the expression of lipopolysaccharide-binding protein in murine white adipose tissue.Bioscience of microbiota, food and health · 2022Article
- Targeting programmed cell death in metabolic dysfunction-associated fatty liver disease (MAFLD): a promising new therapy.Cellular & molecular biology letters · 2021Review
- Article
- Article
- Bile Acid Sequestrant, Sevelamer Ameliorates Hepatic Fibrosis with Reduced Overload of Endogenous Lipopolysaccharide in Experimental Nonalcoholic Steatohepatitis.Microorganisms · 2020Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various rodent models have been proposed for basic research; however, the pathogenesis of human nonalcoholic steatohepatitis (NASH) is difficult to closely mimic. Lipopolysaccharide (LPS) has been reported to play a pivotal role in fibrosis development during NASH progression via activation of toll-like receptor 4 (TLR4) signaling. This study aimed to clarify the impact of low-dose LPS challenge on NASH pathological progression and to establish a novel murine NASH model. C57BL/6J mice were fed a choline-deficient l-amino-acid-defined (CDAA) diet to induce NASH, and low-dose LPS (0.5 mg/kg) was intraperitoneally injected thrice a week. CDAA-fed mice showed hepatic CD14 overexpression, and low-dose LPS challenge enhanced TLR4/NF-κB signaling activation in the liver of CDAA-fed mice. LPS challenge potentiated CDAA-diet-mediated insulin resistance, hepatic steatosis with upregulated lipogenic genes, and F4/80-positive macrophage infiltration with increased proinflammatory cytokines. It is noteworthy that LPS administration extensively boosted pericellular fibrosis with the activation of hepatic stellate cells in CDAA-fed mice. Exogenous LPS administration exacerbated pericellular fibrosis in CDAA-mediated steatohepatitis in mice. These findings suggest a key role for LPS/TLR4 signaling in NASH progression, and the authors therefore propose this as a suitable model to mimic human NASH.
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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.