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.
1Humboldt University, Charité Hospital, Laboratory for Molecular Genetics, Polymicrobial Infections and Bacterial Biofilms, 10098 Berlin, Germany
2Centre of Excellence for Gastrointestinal Inflammation and Immunity Research, University of Alberta, Edmonton, Alberta, Canada
3University Poliklinik, Berlin, Germany
4Faculty of Medicine and Health Sciences, Ghent University, Ghent University Hospital, Ghent, Belgium
Reprints: Alexander Swidsinski, Humboldt University, Charité Hospital, Laboratory for Molecular Genetics, Polymicrobial Infections and Bacterial Biofilms, 10098 Berlin, Germany
Received for publication August 15 2008; Accepted August 18 2008
Published online 9 October 2008 in Wiley InterScience (www.interscience.wiley.com).