Liver fibrosis is characterized by an excessive deposition of extracellular matrix proteins that occurs in chronic liver disease of any origin including fatty liver disease, viral hepatitis, alcohol abuse or inherited diseases. Cirrhosis occurs with the development of regenerating nodules of hepatocytes. Patients with decompensated liver cirrhosis have a poor prognosis and liver transplantation is often necessary. There are no effective anti-fibrotic treatments for patients with chronic liver diseases.
Changes in the intestinal microflora and bacterial translocation are common in patients with liver disease, and there is strong evidence that the translocation of bacteria and their products across the leaky gut barrier contributes to the progression of liver fibrosis. Supporting evidence comes from animal studies demonstrating that intestinal decontamination is associated with decreased liver fibrogenesis. Despite this strong association, the exact molecular mechanism of how changes in the enteric microbiome and bacterial translocation contribute to liver disease progression remains unknown.
In our laboratory we study host factors that mediate chronic liver diseases. In addition, we focus on microbial factors that change in response to liver injury and chronic liver disease and the consequences of intestinal dysbiosis on host biology. We specifically are interested in the enteric microbiome, metagenome and transcriptome associated with liver disease.
We use in vitro and in vivo technologies to study various aspects of chronic liver disease. We specifically use animal models mimicking fatty liver disease, alcoholic and non-alcoholic steatohepatitis, toxic and cholestatic models of liver disease.
In addition, a very important part of our laboratory is a translational aspect to identify targets for therapy and to generate interventions that are able to prevent or treat liver disease in patients.