Leader: Laurent Dubuquoy
Alcoholic hepatitis (AH), the most severe form of liver damage due to alcohol, is associated with a high risk of infections and premature death.
Its pathophysiology is poorly understood due to the lack of relevant animal models and because of the scarcity of human samples available. Our recent work suggests that the pathogenesis of AH lies in a complex balance between inflammation, cell death, tissue repair and regeneration of the liver. This balance appears broken in AH patients mainly due to a deep alteration of the liver regeneration and more specifically of the hepatocyte compartment. The main objective of our research program is to better understand the pathogenesis of AH and identify the main mechanisms leading to death, in order to develop future targeted therapies.
In parallel, we are interested in the role of an innate immunity receptor, NOD1, in neutrophil-dependent liver injury. Our goal is to decipher the cellular and molecular mechanisms targeted by NOD1, both in neutrophils and hepatocytes, leading to the modulation of inflammatory lesions in the liver.