Furthermore, confirming the fact that GPBAR1 functions as a braking mechanism for intestinal inflammation [23], mice harboring a disrupted Gpbar1 develop a progressive inflammation with age and were more prone to develop severe disease than their wild type counterparts when challenged with TNBS, as shown by assessing the colitis activity score (CDAI) and expression of Tnf-α and Il-1β mRNA, and this pattern associated with a very robust induction of Ace2 mRNA expression in the colon. This evidence concerns the gene TNF and colitis.