Cited by 158Liver physiology and pathologyImmune Response and InflammationLiver Diseases and Immunity

Toll-like Receptor 4 and Hepatic Fibrogenesis

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Pradere, Jean-Philippe, Troeger, Juliane, Dapito, Dianne, Mencin, Ali, Schwabe, Robert·2010·Seminars in Liver Disease

Abstract

Inflammation is strongly associated with chronic hepatic injury and the ensuing wound-healing process. Recent evidence from mouse models and human studies implicates Toll-like receptors (TLRs) as important regulators of the inflammatory response and a functional link between inflammation and fibrosis in the chronically injured liver. Here, we review mechanisms by which TLR4 and TLR4 ligands from the intestinal microbiota contribute to hepatic injury, inflammation, hepatic stellate cell activation, and fibrosis.

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Crossref · 10.1055/s-0030-1255353

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  • Serum lipopolysaccharide levels are increased in patients with chronic alcohol abuse.

    “Likewise, serum LPS levels are increased in patients with chronic alcohol abuse16.”
  • A single alcohol binge increases bacterial translocation, with portal blood lipopolysaccharide in rats rising from undetectable levels to 30-80 pg/ml after ethanol administration.

    “Even a single binge of alcohol is sufficient to increase bacterial translocation, as evidenced by an increase of LPS in portal blood rats from undetectable levels to 30–80 pg/ml after ethanol administration 16.”
  • The gut microbiota makes a key contribution to early alcoholic liver disease.

    “The key contribution of the gut microbiota to early stages of ALD has been firmly established in the past two decades.”
  • Gut microbiota alterations occur in earlier stages of liver disease and in animal models.

    “Likewise, a number of studies have demonstrated alterations of the gut microbiota in earlier stages of liver disease 35,36 as well as in animal models16,31.”

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  1. [72]Bataller R Brenner DA Liver fibrosis J Clin Invest 2005 115 2 209 218 15690074 PMC546435

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Authors
Pradere, J.-P., Troeger, J., Dapito, D., Mencin, A., & Schwabe, R.
Affiliations
Columbia University (US)
Venue
Seminars in Liver Disease
Published
2010-07-21
Volume
30
Issue
03
Pages
232-244
ISSN
  • 0272-8087 (ISSN-L)
  • 1098-8971
OpenAlex
W1988345602
Cited by
158
References
117
Citations by year
2026: 4 · 2025: 7 · 2024: 10 · 2023: 8 · 2022: 14 · 2021: 16 · 2020: 18 · 2019: 6 · 2018: 7 · 2017: 13 · 2016: 2 · 2015: 12 · 2014: 4 · 2013: 11 · 2012: 13
FWCI
7.54
Type
journal article
Language
en
Open access
Locations
  • Seminars in Liver Disease (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (5u54ca126513-03)
  • National Cancer Institute (U54CA163111, U54 CA126513.)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK076920)
Topics
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
Keywords
TLR4, liver fibrosis, liver inflammation, chronic liver injury, hepatic stellate cell activation, gut microbiota, TLR4 ligands, wound healing
MeSH terms
Animals, Extracellular Matrix, Hepatitis, Humans, Ligands, Liver, Liver Cirrhosis, Signal Transduction, Inflammation Mediators, Toll-Like Receptor 4, Hepatic Stellate Cells

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