TITLE

Increased Transmucosal Uptake of E. coli K12 in Collagenous Colitis Persists After Budesonide Treatment

AUTHOR(S)
Münch, Andreas; Söderholm, Johan D; Öst, Åke; Ström, Magnus
PUB. DATE
March 2009
SOURCE
American Journal of Gastroenterology;Mar2009, Vol. 104 Issue 3, p679
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
OBJECTIVES:Collagenous colitis is increasingly recognized as a common diarrheal disorder of inflammatory origin. Intestinal inflammation is generally associated with increased mucosal permeability, but little is known about barrier function in microscopic colitis. Our aim was to investigate the mucosal barrier to nonpathogenic bacteria in collagenous colitis.METHODS:The study included 33 individuals, 25 with collagenous colitis (14 in clinical remission, 11 with active disease, and 8 of these again after 6 weeks budesonide treatment) and 8 control patients. Bowel movements were registered for 1 week. Endoscopic biopsies from the sigmoid colon were mounted in modified Ussing chambers and assessed for short-circuit current (Isc), transepithelial resistance (TER), and transmucosal passage of chemically killed Escherichia coli K12.RESULTS:Bacterial uptake was increased in patients in remission, 1.6 U (1.1–3.0) and in those with active disease, 4.6 U (2.5–5.8; median (IQR)), compared to controls, 0.7 U (0.1–1.1; P=0.004 and P–0.001, respectively). Active disease also had signifi cant decrease in transepithelial resistance (TER) after 120 min, −9.7 Ω cm2 ((−13)−(−4.3)), compared to controls, −5.2 Ω cm2 ((−7.2)−(−3.1)), P−0.03; or patients in remission, −4.8 Ω cm2 ((−8.0)−(−1.2)), P=0.04. Budesonide decreased median stool frequency to 1.9 (1.3–2.2) compared to 3.8 (3.7–4.2) before treatment (P=0.01), but bacterial uptake was still increased after budesonide 2.9 U (1.5–3.8), (P=0.006 compared to controls), and there were no significant changes in histology.CONCLUSIONS:Collagenous colitis presents with significantly increased uptake and altered mucosal reactivity to nonpathogenic bacteria. Budesonide induces clinical remission and restores mucosal reactivity but does not abolish the increased bacterial uptake. An underlying barrier dysfunction may explain the frequent and rapid relapses in CC.Am J Gastroenterol 2009; 104: 679–685; doi:10.1038/ajg.2008.95; published online 10 February 2009
ACCESSION #
36803351

 

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