Administration of a potent FXR agonist, obeticholic acid (4; Figure 2), to a high-fat diet CDI mouse model resulted in a reduced C. difficile burden, as well as reduced diarrhea and improved intestinal inflammation [99]; similarly, treatment of a mouse CDI model with the tertiary bile acid, ursodeoxycholic acid (UDCA), resulted in increased FXR-related transcripts and associated reduced intestinal inflammation [100]. Here, NR1H4 is linked to clostridium difficile infection.