Open AccessBacterial overgrowth and inflammation of small intestine after carboxymethylcellulose ingestion in genetically susceptible mice
Author(s) -
Swidsinski Alexander,
Ung Victoria,
Sydora Beate C.,
LoeningBaucke Vera,
Doerffel Yvonne,
Verstraelen Hans,
Fedorak Richard N.
Publication year - 2009
Publication title -
inflammatory bowel diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.932
H-Index - 146
eISSN - 1536-4844
pISSN - 1078-0998
DOI - 10.1002/ibd.20763
Subject(s) - bacteria , inflammation , mucus , microbiology and biotechnology , ingestion , inflammatory bowel disease , biology , intestinal mucosa , disease , medicine , immunology , pathology , endocrinology , ecology , genetics
Abstract Background: Detergents and emulsifiers added to food may destroy the mucus barrier, which normally isolates bacteria from the intestinal wall, and lead to chronic bowel inflammation in susceptible persons. We investigated the influence of 2% carboxymethylcellulose (CMC) on the biostructure of the intestinal microbiota in IL‐10 gene‐deficient mice. Methods: Twenty to 27‐week‐old IL‐10 gene‐deficient mice received either 2% CMC solution ( n = 7) or water ( n = 6) orally for 3 weeks. Intestinal bacteria were investigated using fluorescence in situ hybridization in paraffin‐fixed sections of the intestine. Results: CMC‐treated IL‐10 gene‐deficient mice demonstrated a massive bacterial overgrowth, distention of spaces between villi, with bacteria filling these spaces, adherence of bacteria to the mucosa, and migration of bacteria to the bottom of the crypts of Lieberkuehn. Leukocytes migrated into the intestinal lumen in 4 of the 7 CMC mice. The changes were similar to those observed in Crohn's disease in humans and were absent in control animals. Conclusions: CMC induces bacterial overgrowth and small bowel inflammation in susceptible animals. Because of its ubiquity in products and its unrestricted use in food of the industrial world, CMC is an ideal suspect to account for the rise of IBD in the 20th century. (Inflamm Bowel Dis 2008)