Low Levels of Bile Acids Increase Bacterial Uptake in Colonic biopsies from Collagenous Colitis Patients in Remission

• Published in: Alimentary pharmacology & therapeutics 2011-03, Vol.33 (8)
• Main Authors: Münch, Andreas, Soderholm, Johan D, Öst, Åke, Carlsson, Anders, Magnusson, Karl-Eric, Ström, Magnus
• Format: Article
• Language: English
• ISSN: 0269-2813; 1365-2036
• DOI: 10.1111/j.1365-2036.2011.04611.x

Background: Patients with collagenous colitis (CC) have an impaired mucosal barrier. Moreover, CC is associated with bile acid malabsorption. Bile acids can increase bacterial mucosal uptake in humans. Mucosal barrier function was investigated by exposing colonic biopsies to chenodeoxycholic acid (CDCA) or deoxycholic acid (DCA) in Ussing chamber experiments. Methods: The study comprised 33 individuals; 25 with CC (14 in clinical remission without treatment, 11 with active disease, and 10 examined in clinical remission resulting from treatment with 6 mg budesonide); 8 healthy individuals undergoing screening colonoscopy served as controls. Endoscopic biopsies from the sigmoid colon were mounted in modified Ussing chambers and assessed for short circuit current (Isc), potential difference (PD), transepithelial resistance (TER), and transmucosal passage of E. coli K12 after adding 100 µmol/l CDCA or DCA. Results: When adding 100 µmol/l CDCA or DCA, bacterial uptake increased 4-fold in biopsies of patients in remission; CDCA 6.5 units [2.5-9.8] and DCA 6.2 units [2.1-22] (median [IQR]), compared with uptake in biopsies without added bile acids 1.6 units [1.1-3]; (p=0.004 and p=0.01, respectively). In active disease and in patients in remission due to budesonide treatment, bile acids did not affect bacterial uptake. Confocal microscopy revealed transepithelial passage of E.coli K12 within 30 min. Conclusions: Low concentrations of dihydroxy-bile acids exacerbate mucosal barrier dysfunction in colonic biopsies of patients with CC in remission. This allows a substantially increased bacterial uptake, which may contribute to recurrence of inflammation.