Activation of bile salt nuclear receptor FXR is repressed by pro-inflammatory cytokines activating NF-κB signalling in the intestine

Raffaella M. Gadaleta (1, 2) , Bas Oldenburg (1) , Ellen C.L. Willemsen (2) , Maureen Spit (2) , Stefania Murzilli , Lorena Salvatore , Leo W.J. Klomp (2) , Peter D. Siersema (1) , Karel J. van Erpecum (1) , Saskia W.C. van Mil (2)

1 Department of Gastroenterology and Hepatology
2 Department of Metabolic and Endocrine Diseases

Hyperactivation of NF-κB is a key factor in the pathophysiology of inflammatory bowel disease (IBD). We previously showed that the bile salt nuclear Farnesoid X Receptor (FXR) counter-regulates intestinal inflammation, possibly via repression of NF-κB. Here, we examine whether mutual antagonism between NF-κB and FXR exists.

Mots clés: Inflammatory bowel disease; Nuclear Factor κB; Farnesoid X Receptor; mutual inhibition

Domaines: Biochimie, Biologie Moléculaire

Raffaella M. Gadaleta, Bas Oldenburg, Ellen C.L. Willemsen, Maureen Spit, Stefania Murzilli, et al.. Activation of bile salt nuclear receptor FXR is repressed by pro-inflammatory cytokines activating NF-κB signalling in the intestine. Biochimica et Biophysica Acta - Molecular Basis of Disease, 2011, ⟨10.1016/j.bbadis.2011.04.005⟩. ⟨hal-00706530⟩