title: Systematic review: bile acids and intestinal inflammation-luminal aggressors or regulators of mucosal defence?
abstract: BACKGROUND
  Inflammatory bowel diseases (IBD), comprising Crohn's disease and ulcerative colitis (UC), are chronic conditions attributed to an aberrant immune response to luminal triggers. Recently, published work suggests a pathogenic role for bile acids in this context.
  
  
  OBJECTIVE
  To perform a systematic review of studies investigating the role of bile acids in intestinal inflammation and present potentially relevant clinical implications.
  
  
  METHODS
  Pubmed search for English language articles published up to May 2015. Terms used were: 'bile', 'bile acid', 'barrier', 'small bowel injury', 'Crohn's' and 'colitis'.
  
  
  RESULTS
  Experimental studies support a variable role for bile acids in intestinal barrier homoeostasis. This may be attributed to different physicochemical properties, variable effects on epithelia and immune cells via bile acids-specific receptors, or through a cross-talk with the gut microbiome. A reduction in the bile acids pool, with lower concentrations of secondary forms, has been recognised for some time in Crohn's disease and associated to ileal dysfunction and bile acids malabsorption. Recent work suggests that these changes, including an increase in sulphated forms, are related to inflammatory activity in both Crohn's disease and UC. The detrimental effects of 'western diet' elements such as emulsifiers and fat, which have been implicated in the development of the current IBD and obesity epidemics, may also be bile acid-mediated.
  
  
  CONCLUSIONS
  Although there are only a few observational clinical studies to support an interaction, in vivo human and animal studies support an association between bile acids metabolism, the gut microbiome and intestinal inflammation. This may well prove to have significant diagnostic and therapeutic implications.
authors.affiliation: Department of Gastroenterology, King's College Hospital, London, UK.
authors.forename: P
authors.initials: P
authors.lastname: Pavlidis
authors.affiliation: Division of Transplantation and Mucosal Biology, King's College London, London, UK.
authors.forename: N
authors.initials: N
authors.lastname: Powell
authors.affiliation: Department of Biochemistry, King's College Hospital, London, UK.
authors.forename: R P
authors.initials: RP
authors.lastname: Vincent
authors.affiliation: Centre of Host-Microbiome Interactions, King's College London, London, UK.
authors.forename: D
authors.initials: D
authors.lastname: Ehrlich
authors.affiliation: Department of Gastroenterology, King's College Hospital, London, UK.
authors.forename: I
authors.initials: I
authors.lastname: Bjarnason
authors.affiliation: Department of Gastroenterology, King's College Hospital, London, UK.
authors.forename: B
authors.initials: B
authors.lastname: Hayee
mesh_terms: D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D003093:Colitis, Ulcerative / Q000276:immunology* / Q000517:prevention & control; D003424:Crohn Disease / Q000276:immunology* / Q000517:prevention & control; D000069196:Gastrointestinal Microbiome / Q000276:immunology / Q000502:physiology; D006801:Humans; D007082:Ileum / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology
chemical_list: D001647:Bile Acids and Salts