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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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The biliary system of the liver, crucial for bile secretion and drug excretion, comprises intrahepatic bile ducts that merge to form the common hepatic duct. This duct, carrying hepatic bile, combines with the cystic duct, draining the gallbladder and forming the common bile duct, which empties into the duodenum. Bile, produced by hepatic cells lining the bile canaliculi, is composed primarily of water, bile salts, pigments, electrolytes, and lesser amounts of cholesterol and fatty acids. Bile...
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Related Experiment Video

Updated: Nov 9, 2025

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Intestinal microbiota drives cholestasis-induced specific hepatic gene expression patterns.

Oriol Juanola1, Mohsin Hassan2, Pavitra Kumar3

  • 1Translational Research Laboratory, Gastroenterology and Hepatology, Ente Ospedaliero Cantonale, Università Della Svizzera Italiana, Lugano, Switzerland.

Gut Microbes
|April 13, 2021
PubMed
Summary

The absence of gut microbiota worsens liver injury in acute cholestasis. However, the presence of intestinal bacteria offers partial protection by modulating hepatic gene expression, suggesting microbiota-targeted therapies for liver disease.

Keywords:
Intestinal microbiotaacute cholestasisbile acidsgene expressiongerm-free micemetabolism

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Area of Science:

  • Gastroenterology and Hepatology
  • Microbiology
  • Immunology

Background:

  • Intestinal microbiota influences host metabolism and immunity, impacting the gut-liver axis.
  • Alterations in gut microbiota composition can affect the severity of liver diseases.
  • Mechanisms linking gut microbiota to liver disease pathogenesis are not fully understood.

Purpose of the Study:

  • To investigate the role of intestinal microbiota in acute cholestasis.
  • To compare liver injury outcomes in germ-free (GF) versus conventionally colonized mice.
  • To elucidate the impact of microbiota on hepatic gene expression, inflammation, and metabolism during cholestasis.

Main Methods:

  • Acute cholestasis induced by bile duct ligation (BDL) in GF and altered Schaedler's flora (ASF) mice.
  • Analysis of hepatic histology, gene expression, inflammation markers, lipid metabolism, and mitochondrial function 5 days post-BDL.
  • Quantification of plasma bile acids (BA) using UHPLC-HRMS.

Main Results:

  • GF mice exhibited aggravated liver injury and bile infarcts after BDL compared to ASF mice.
  • GF mice showed altered baseline gene expression related to amino and fatty acid metabolism.
  • Post-BDL, ASF mice displayed increased ductular reactions, proliferation, collagen deposition, and autophagy; GF mice showed heightened hepatic inflammation (e.g., increased IL-1β, osteopontin) and MAPK pathway activation.
  • Microbiota presence partially protected mitochondrial function and fatty acid metabolism.

Conclusions:

  • Germ-free conditions exacerbate liver injury in acute cholestasis, while intestinal microbiota confers partial protection.
  • Protective effects are linked to distinct hepatic gene expression profiles related to tissue repair, metabolism, and immunity.
  • Modulating the intestinal microbiota may offer novel therapeutic strategies for cholestatic liver diseases.