Marlies Meisel, PhD*
W1048 Biomedical Science Tower
200 Lothrop Street
Pittsburgh, PA 15261
Aging is associated with an increased incidence of cancer, cardiovascular diseases and other detrimental inflammatory diseases as well as bacterial translocation. We could identify that spontaneous gut bacterial translocation is required to initiate myeloid cancer via an IL-6 dependent mechanism in mice deficient of an epigenetic regulator [Meisel et al., Nature 2018].
Liver disease is the result of chronic liver damage from various etiologies including alcohol abuse, obesity, viral hepatitis or is of idiopathic origin and affects several million people in the United States. Early stages are reversible, however chronic inflammatory liver disease may progress to cirrhosis (eventually requiring a liver transplant) which can progress to hepatocellular cancer, an irreversible end stage disease and major cause of morbidity and mortality in the United States.
Despite the fact that hepatic disease is a major health concern, and microbial signals correlate with disease severity, so far there are only few studies that mechanistically demonstrate the impact of systemic microbial signals on the development of liver disease and fibrosis. Yet several questions remain un addressed.
One major goal of my lab is to investigate the underlying mechanisms how microbial signals impact on liver disease development. We will study the local hepatic microbiome (culturing, imaging and sequencing approaches) and the impact of specific microbes (mono-colonizations of germ free mice) on liver immunity and in liver disease development.
Department of Immunology