title: Bacterial-dependent up-regulation of intestinal bile acid binding protein and transport is FXR-mediated following ileo-cecal resection.
abstract: BACKGROUND
  Bile acid (BA) reclamation following ileo-cecal resection (ICR) may prevent colonic mucosa from chronic injury. In this study, we hypothesized that in a murine model of ICR the remnant colon would upregulate the cellular machinery necessary for BA reclamation and would do so in an FXR- and bacteria-dependent manner.
  
  
  METHODS
  Conventional (WT), conventional FXR knockout (FXR null) and germ-free (GF) mice were randomized to undergo either ICR or sham operation. The ascending colon was harvested for histology and immunohistochemistry and changes in bile acid homeostatic gene expression determined by real-time polymerase chain reaction (RT-PCR) 7 days following surgery.
  
  
  RESULTS
  Following ICR WT mice showed significant increases in the expression of genes regulating bile acid transport including IBABP, Asbt, Ost beta and FGF 15. Increased expression of IBABP and Asbt was confirmed by immunohistochemistry. Induction of bile acid transport genes was absent or attenuated in FXR null and GF mice.
  
  
  CONCLUSIONS
  Bacterial dependent up regulation of IBABP is FXR mediated in the colon following ICR. Mice lacking microbiota (GF) or FXR are unable to increase the expression of IBABP or FGF 15.
authors.affiliation: University of North Carolina-Chapel Hill, Chapel Hill, NC, USA.
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Dekaney
authors.forename: Douglas C
authors.initials: DC
authors.lastname: von Allmen
authors.forename: Aaron P
authors.initials: AP
authors.lastname: Garrison
authors.forename: Rachael J
authors.initials: RJ
authors.lastname: Rigby
authors.forename: P Kay
authors.initials: PK
authors.lastname: Lund
authors.forename: Susan J
authors.initials: SJ
authors.lastname: Henning
authors.forename: Michael A
authors.initials: MA
authors.lastname: Helmrath
mesh_terms: D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism; D001692:Biological Transport; D002432:Cecum / Q000601:surgery*; D003106:Colon / Q000378:metabolism / Q000382:microbiology*; D004268:DNA-Binding Proteins / Q000502:physiology*; D005856:Germ-Free Life; D006913:Hydroxysteroid Dehydrogenases / Q000378:metabolism*; D007082:Ileum / Q000601:surgery*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D029363:Organic Anion Transporters, Sodium-Dependent / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000502:physiology*; D027981:Symporters / Q000378:metabolism; D014157:Transcription Factors / Q000502:physiology*; D015854:Up-Regulation; D000099150:Receptor, Farnesoid X-Activated; D045002:3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)
chemical_list: D001647:Bile Acids and Salts; D004268:DNA-Binding Proteins; D006913:Hydroxysteroid Dehydrogenases; D029363:Organic Anion Transporters, Sodium-Dependent; D018160:Receptors, Cytoplasmic and Nuclear; D027981:Symporters; D014157:Transcription Factors; D000099150:Receptor, Farnesoid X-Activated; C071908:sodium-bile acid cotransporter; C435496:AKR1C2 protein, human; D045002:3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)