Devisscher lab

Prof. dr. Lindsey Devisscher

Research topic

“The liver is structurally and functionally positioned as a filter and homeostatic guardian between the gut and the rest of the body. The liver drains gut-derived compounds via the portal tract, has important tolerogenic and detoxifying functions, controls glucose levels and lipid metabolism and excretes bile acids via the biliary tree to complete the enterohepatic cycle. This cycle is important as it is also involved in the pharmacological effect of drugs and metabolites. Any substance that crosses the intestinal barrier and enters the portal circulation can affect liver homeostasis and vice versa, the liver also communicates with the gut via the capillary system. Unsurprisingly, the liver-gut axis is compromised in many gastrointestinal diseases.

The Gut-Liver ImmunoPharmacology (GLIPh) unit focusses on the role of macrophages, and their potential as therapeutic targets, in the gut-liver crosstalk in the context of chronic liver diseases. Chronic liver diseases are all characterized by a leaky-gut and intestinal microbial dysbiosis. As a consequence, the hepatic immune system is chronically activated by gut-derived bacterial compounds and this results in chronic hepatic inflammation. Chronic inflammation in the liver induces pathological vessel and scar formation and results in associated complications such as portal hypertension which further compromise the liver-gut cross-talk. As such, patients with chronic liver diseases are at increased risk for bacterial translocation and sepsis. Altering intestinal microbiota, the bile acid pool and intestinal motility have all become explorative novel therapeutic strategies in patients suffering from chronic liver diseases but despite this, effective therapy is lacking. By using mouse models, human samples obtained via close collaboration with the Hepatology Research Unit (headed by Prof. Hans Van Vlierberghe) and in vitro assays, we explore the causal role of macrophages in the disturbed gut-liver crosstalk and explore new therapeutic opportunities which target macrophages and inflammation to restore the liver-gut symbiosis in chronic liver disease.”

Areas of expertise

  • In vitro assays and mouse models for gut and liver diseases including acute and chronic colitis models, paracetamol-induced acute liver injury, alcoholic and non-alcoholic fatty liver disease and associated liver inflammation, cholestatic liver disease, models for liver fibrosis and hepatocellular carcinoma
  • Liver and gut immunology

Selected publications

  1. Devisscher et al. The role of macrophages in obesity-driven chronic liver disease. J Leukoc Biol. 2016
  2. Devisscher et al. Targeting the angio-proteostasis network: Combining the forces against cancer. Pharmacol Ther. 2016
  3. Paridaens et al. . Combination of tauroursodeoxycholic acid and N-acetylcysteine exceeds standard treatment for acetaminophen intoxication. Liver Int. 2016
  4. Raevens et al. Inhibition of placental growth factor targets pulmonary angiogenesis and serves as therapeutic strategy for hepatopulmonary syndrome in mice. Hepatology. 2018
  5. Devisscher et al. Non-alcoholic steatohepatitis induces transient changes within the liver macrophage pool. Cell Immunol. 2017
  6. Lefere et al. Angiopoietin-2 promotes pathological angiogenesis and is a novel therapeutic target in murine non-alcoholic fatty liver disease. Hepatology. 2018
  7. Van Campenhout et al. Common Bile Duct Ligation as Model for Secondary Biliary Cirrhosis. Methods Mol Biol. 2019
  8. Lefere et al. Unveiling the depletion of Kupffer cells in experimental hepatocarcinogenesis through liver macrophage subtype-specific markers. J Hepatol. 2019
  9. Raevens et al. Combination of sivelestat and N-acetylcysteine alleviates the inflammatory response and exceeds standard treatment for acetaminophen-induced liver injury. J Leukoc Biol. 2019

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