Leader: Benjamin Bertin
The pathophysiology of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC) is multifactorial involving genetic, environmental, microbial and immunological components. One of the most commonly accepted hypothesis to explain the origin of IBD is the breaking of a critical balance in the intestine: oral tolerance. According to this hypothesis, the body reacts abnormally and uncontrollably against antigens from the intestinal lumen which are usually "invisible" to the immune system.
Many studies, including ours, have revealed the essential role of a family of transcription factors, nuclear receptors in regulating the intestinal homeostasis. The aim of our research is to characterize the role of some of these nuclear receptors and their ligands (PPAR, peroxisome proliferator activated receptor gamma; LRH-1, Liver Receptor Homolog-1) in normal and pathological conditions (inflammatory and / or metabolic), with a particular interest in the intestinal epithelial cell. The description of the cellular and molecular events causing malfunctions of intestinal physiology opens up the perspective of identifying new therapeutic approaches in the field of IBD, metabolic diseases or cancer.
Publications
Louvet A, Labreuche J, Artru F, et al. Main drivers of outcome differ between short term and long term in severe alcoholic hepatitis: A prospective study. Hepatology 2017;66:1464-1473.
Guerbau L, Gerard R, Duveau N, et al. Patients with Crohn's Disease with High Body Mass Index Present More Frequent and Rapid Loss of Response to Infliximab. Inflamm Bowel Dis 2017;23:1853-1859.
Fumery M, Speca S, Langlois A, et al. Peroxisome proliferator-activated receptor gamma (PPARgamma) regulates lactase expression and activity in the gut. EMBO Mol Med 2017;9:1471-1481.
Speca S, Rousseaux C, Dubuquoy C, et al. Novel PPARgamma Modulator GED-0507-34 Levo Ameliorates Inflammation-driven Intestinal Fibrosis. Inflamm Bowel Dis 2016;22:279-92.
Driss V, El Nady M, Delbeke M, et al. The schistosome glutathione S-transferase P28GST, a unique helminth protein, prevents intestinal inflammation in experimental colitis through a Th2-type response with mucosal eosinophils. Mucosal Immunol 2016;9:322-35.