Altered Fecal Bile Acid Pattern in Patients with Inflammatory Bowel Disease

Digestion ◽  
1986 ◽  
Vol 35 (4) ◽  
pp. 189-198 ◽  
Author(s):  
W. Kruis ◽  
H.-D. Kalek ◽  
F. Stellaard ◽  
G. Paumgartner
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Bowel Disease ◽  
Fecal Bile Acid ◽  
Inflammatory Bowel

scholarly journals Serum bile acid profiling reflects enterohepatic detoxification state and intestinal barrier function in inflammatory bowel disease

2009 ◽  
Vol 15 (25) ◽  
pp. 3134 ◽  
Author(s):  
Carsten Gnewuch ◽  
Gerhard Liebisch ◽  
Thomas Langmann ◽  
Benjamin Dieplinger ◽  
Thomas Mueller ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Bowel Disease ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Serum Bile Acid ◽  
Inflammatory Bowel

scholarly journals A Pilot Integrative Analysis of Colonic Gene Expression, Gut Microbiota, and Immune Infiltration in Primary Sclerosing Cholangitis-Inflammatory Bowel Disease: Association of Disease With Bile Acid Pathways

2020 ◽  
Vol 14 (7) ◽  
pp. 935-947 ◽  
Author(s):  
Mohammed Nabil Quraishi ◽  
Animesh Acharjee ◽  
Andrew D Beggs ◽  
Richard Horniblow ◽  
Chris Tselepis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Gut Microbiota ◽  
Primary Sclerosing Cholangitis ◽  
Bowel Disease ◽  
Sclerosing Cholangitis ◽  
16S Rrna Analysis ◽  
Immune Infiltration ◽  
Inflammatory Bowel

Abstract Background Although a majority of patients with PSC have colitis [PSC-IBD; primary sclerosing cholangitis-inflammatory bowel disease], this is phenotypically different from ulcerative colitis [UC]. We sought to define further the pathophysiological differences between PSC-IBD and UC, by applying a comparative and integrative approach to colonic gene expression, gut microbiota and immune infiltration data. Methods Colonic biopsies were collected from patients with PSC-IBD [n = 10], UC [n = 10], and healthy controls [HC; n = 10]. Shotgun RNA-sequencing for differentially expressed colonic mucosal genes [DEGs], 16S rRNA analysis for microbial profiling, and immunophenotyping were performed followed by multi-omic integration. Results The colonic transcriptome differed significantly between groups [p = 0.01]. Colonic transcriptomes from HC were different from both UC [1343 DEGs] and PSC-IBD [4312 DEGs]. Of these genes, only 939 had shared differential gene expression in both UC and PSC-IBD compared with HC. Imputed pathways were predominantly associated with upregulation of immune response and microbial defense in both disease cohorts compared with HC. There were 1692 DEGs between PSC-IBD and UC. Bile acid signalling pathways were upregulated in PSC-IBD compared with UC [p = 0.02]. Microbiota profiles were different between the three groups [p = 0.01]; with inferred function in PSC-IBD also being consistent with dysregulation of bile acid metabolism. Th17 cells and IL17-producing CD4 cells were increased in both PSC-IBD and UC when compared with HC [p < 0.05]. Multi-omic integration revealed networks involved in bile acid homeostasis and cancer regulation in PSC-IBD. Conclusions Colonic transcriptomic and microbiota analysis in PSC-IBD point toward dysregulation of colonic bile acid homeostasis compared with UC. This highlights important mechanisms and suggests the possibility of novel approaches in treating PSC-IBD.

Sa1785 - The Association of Serum 7A Hydroxy 4 Cholesten 3 One (7C4) with Bile Acid Diarrhea in Patients with Inflammatory Bowel Disease

2018 ◽  
Vol 154 (6) ◽  
pp. S-393
Author(s):  
Robert Battat ◽  
Marjolijn Duijvestein ◽  
Niels Vande Casteele ◽  
Siddharth Singh ◽  
Mark Renshaw ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals P246 The association of serum 7α-hydroxy-4-cholesten-3-one (7C4) with Bile Acid Diarrhoea in patients with inflammatory bowel disease

2018 ◽  
Vol 12 (supplement_1) ◽  
pp. S224-S225
Author(s):  
R Battat ◽  
M Duijvestein ◽  
N Vande Casteele ◽  
S Singh ◽  
M Renshaw ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Glucocorticoids differentially regulate Na-bile acid cotransport in normal and chronically inflamed rabbit ileal villus cells

2010 ◽  
Vol 298 (5) ◽  
pp. G675-G682 ◽  
Author(s):  
Steven Coon ◽  
Ramesh Kekuda ◽  
Prosenjit Saha ◽  
Uma Sundaram
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Western Blot ◽  
Bowel Disease ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Kinetic Studies ◽  
Rabbit Ileum ◽  
Expression Levels ◽  
Inflammatory Bowel

Previous studies have demonstrated that apical Na-bile acid cotransport (ASBT) is inhibited during chronic ileitis by both a decrease in the affinity as well as a decrease in the number of cotransporters. Methylprednisolone (MP), a commonly used treatment for inflammatory bowel disease (IBD, e.g., Crohn's disease), has been shown to reverse the inhibition of several other Na-solute cotransporters during chronic enteritis. However, the effect of MP on ASBT in the chronically inflamed ileum is not known. MP stimulated ASBT in villus cells from the normal rabbit ileum by increasing the cotransporter expression without a change in the affinity of the cotransporter for bile acid. Western blot studies demonstrated an increase in cotransporter expression. MP reversed the inhibition of ASBT in villus cells from the chronically inflamed ileum. Kinetic studies demonstrated that the mechanism of MP-mediated reversal of ASBT inhibition was secondary to a restoration of both affinity as well as cotransporter numbers. Western blot analysis demonstrated restoration of cotransporter numbers after MP treatment of rabbits with chronic ileitis. Thus MP stimulates ASBT in the normal ileum by increasing cotransporter numbers. MP reverses the inhibition of ASBT during chronic ileitis. However, MP restores the diminished affinity as well as cotransporter expression levels during chronic ileitis. Thus MP differentially regulates ASBT in the normal and in the chronically inflamed ileum.

Sign in / Sign up

Export Citation Format

Share Document