ArticleCancer prevention research (Philadelphia, Pa.)2012
Gut-derived lipopolysaccharide promotes T-cell-mediated hepatitis in mice through Toll-like receptor 4.
Article in Cancer prevention research (Philadelphia, Pa.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- Understanding crosstalk between the gut and liver microbiome: pathogenesis to therapeutic approaches in liver cancer.Cancer cell international · 2025Review
- Berberine alleviates concanavalin A-induced autoimmune hepatitis in mice by modulating the gut microbiota.Hepatology communications · 2024Article
- RNA mFrontiers in immunology · 2024Review
- The Role of TLR4 in the Immunotherapy of Hepatocellular Carcinoma: Can We Teach an Old Dog New Tricks?Cancers · 2023Review
- Gut Microbiota Regulation of AHR Signaling in Liver Disease.Biomolecules · 2022Review
- Crosstalk between liver macrophages and gut microbiota: An important component of inflammation-associated liver diseases.Frontiers in cell and developmental biology · 2022Review
- Relationship between Intestinal Microflora and Hepatocellular Cancer Based on Gut-Liver Axis Theory.Contrast media & molecular imaging · 2022Review
- Administration ofFrontiers in microbiology · 2019Article
- The Differential Roles of T Cells in Non-alcoholic Fatty Liver Disease and Obesity.Frontiers in immunology · 2019Review
- Toll-like receptor 4: a target for chemoprevention of hepatocellular carcinoma in obesity and steatohepatitis.Oncotarget · 2018Article
- Protective Effect ofFrontiers in microbiology · 2017Article
- Enterogenous bacterial glycolipids are required for the generation of natural killer T cells mediated liver injury.Scientific reports · 2016Article
- Elevated serum soluble CD14 levels in chronic HBV infection are significantly associated with HBV-related hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Innate immunity and hepatocarcinoma: Can toll-like receptors open the door to oncogenesis?World journal of hepatology · 2016Review
- The Fab Fragment of a Human Anti-Siglec-9 Monoclonal Antibody Suppresses LPS-Induced Inflammatory Responses in Human Macrophages.Frontiers in immunology · 2016Article
- Novel insights in preventing Gram-negative bacterial infection in cirrhotic patients: review on the effects of GM-CSF in maintaining homeostasis of the immune system.Hepatology international · 2015Review
- Natural killer T cells play a necessary role in modulating of immune-mediated liver injury by gut microbiota.Scientific reports · 2014Article
- The microbiota regulates susceptibility to Fas-mediated acute hepatic injury.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Lipoic acid suppresses portal endotoxemia-induced steatohepatitis and pancreatic inflammation in rats.World journal of gastroenterology · 2013Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Robust clinical and epidemiologic data support the role of inflammation as a key player in hepatocellular carcinoma (HCC) development. Our previous data showed that gut-derived lipopolysaccharide (LPS) promote HCC development by activating Toll-like receptor 4 (TLR4) expressed on myeloid-derived cells. However, the effects of gut-derived LPS on other types of liver injury models are yet to be studied. The purpose of this study was to determine the importance of gut-derived LPS and TLR4 signaling in a T-cell-mediated hepatitis-Con A-induced hepatitis model, which mimic the viral hepatitis. Reduction of endotoxin using antibiotics regimen or genetic ablation of TLR4 in mice significantly alleviate Con A-induced liver injury by inhibiting the infiltration of T lymphocytes into the liver and the activation of CD4(+) T lymphocytes as well as the production of T helper 1 cytokines; in contrast, exogenous LPS can promote Con A-induced hepatitis and CD4(+) T cells activation in vivo and in vitro. Reconstitution of TLR4-expressing myeloid cells in TLR4-deficient mice restored Con A-induced liver injury and inflammation, indicating the major cell target of LPS. In addition, TLR4 may positively regulate the target hepatocellular apoptosis via the perforin/granzyme B pathway. These data suggest that gut-derived LPS and TLR4 play important positive roles in Con A-induced hepatitis and modulation of the gut microbiotia may represent a new avenue for therapeutic intervention to treat acute hepatitis induced by hepatitis virus infection, thus to prevent hepatocellular carcinoma.
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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.