Cited by 123Liver physiology and pathologyLiver Diseases and ImmunityLiver Disease Diagnosis and Treatment

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LPS signaling enhances hepatic fibrogenesis caused by experimental cholestasis in mice

Isayama, Fuyumi, Hines, Ian N., Kremer, Michael, Milton, Richard J., Byrd, Christy L., Perry, Ashley W., McKim, Stephen E., Parsons, Christopher, Rippe, Richard A., Wheeler, Michael D.·2006·American Journal of Physiology-Gastrointestinal and Liver Physiology

DOI 10.1152/ajpgi.00405.2005

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Abstract

Although it is clear that bile acid accumulation is the major initiator of fibrosis caused by cholestatic liver disease, endotoxemia is a common side effect. However, the depletion of hepatic macrophages with gadolinium chloride blunts hepatic fibrosis. Because endotoxin is a key activator of hepatic macrophages, this study was designed to test the hypothesis that LPS signaling through CD14 contributes to hepatic fibrosis caused by experimental cholestasis. Wild-type mice and CD14 knockout mice (CD14 −/− ) underwent sham operation or bile duct ligation and were killed 3 wk later. Measures of liver injury, such as focal necrosis, biliary cell proliferation, and inflammatory cell influx, were not significantly different among the strains 3 wk after bile duct ligation. Markers of liver fibrosis such as Sirius red staining, liver hydroxyproline, and α-smooth muscle actin expression were blunted in CD14 −/− mice compared with wild-type mice after bile duct ligation. Despite no difference in lymphocyte infiltration, the macrophage/monocyte activation marker OX42 (CD11b) and the oxidative stress/lipid peroxidation marker 4-hydroxynonenal were significantly upregulated in wild-type mice after bile duct ligation but not in CD14 −/− mice. Increased profibrogenic cytokine mRNA expression in the liver after bile duct ligation was significantly blunted in CD14 −/− mice compared with the wild type. The hypothesis that LPS was involved in experimental cholestatic liver fibrosis was tested using mice deficient in LPS-binding protein (LBP −/− ). LBP −/− mice had less liver injury and fibrosis (Siruis red staining and hydroxyproline content) compared with wild-type mice after bile duct ligation. In conclusion, these data demonstrate that endotoxin in a CD14-dependent manner exacerbates hepatic fibrogenesis and macrophage activation to produce oxidants and cytokines after bile duct ligation.

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Authors: Isayama, F., Hines, I. N., Kremer, M., Milton, R. J., Byrd, C. L., Perry, A. W., McKim, S. E., Parsons, C., Rippe, R. A., & Wheeler, M. D.
Affiliations: University of North Carolina at Chapel Hill (US)
ORCID: Hines, Ian N.
Kremer, Michael
Venue: American Journal of Physiology-Gastrointestinal and Liver Physiology
Publisher: American Physiological Society
Published: 2006-06
Volume: 290
Issue: 6
Pages: G1318-G1328
ISSN: 0193-1857 (ISSN-L)
1522-1547
DOI: 10.1152/ajpgi.00405.2005
OpenAlex: W2020219616
Cited by: 123
References: 21
Citations by year: 2026: 2 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 5 · 2021: 3 · 2020: 4 · 2019: 2 · 2018: 8 · 2017: 4 · 2016: 2 · 2015: 8 · 2014: 10 · 2013: 8 · 2012: 15
FWCI: 4.90
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Gastrointestinal and Liver Physiology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
Keywords: liver fibrosis, cholestatic liver disease, lipopolysaccharide signaling, CD14, endotoxemia, hepatic macrophages, bile duct ligation, LPS-binding protein, oxidative stress, 4-hydroxynonenal, alpha-smooth muscle actin, liver injury
MeSH terms: Animals, Cholestasis, Disease Models, Animal, Lipopolysaccharides, Liver, Liver Cirrhosis, Male, Mice, Inbred C57BL, Signal Transduction, Mice, Knockout, Lipopolysaccharide Receptors, Mice

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LPS signaling enhances hepatic fibrogenesis caused by experimental cholestasis in mice

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