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BioMed Research International
Volume 2013 (2013), Article ID 909613, 15 pages
Research Article

Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model

1School of Women’s and Children’s Health, University of New South Wales, Randwick, Sydney, NSW 2031, Australia
2School of Biotechnology and Biomolecular Sciences, University of New South Wales, Randwick, Sydney, NSW 2052, Australia
3Department of Gastroenterology, Sydney Children’s Hospital, Randwick, Sydney, NSW 2031, Australia
4Department of Pathology, Institute of Veterinary, Animal and Biomedical Sciences, Massey University, Palmerston North 4442, New Zealand
5Paediatric Gastroenterology, Christchurch Hospital, Christchurch 8140, New Zealand
6Department of Paediatrics, University of Otago, Christchurch, Christchurch 8140, New Zealand

Received 30 April 2013; Revised 1 July 2013; Accepted 1 July 2013

Academic Editor: David Bernardo

Copyright © 2013 Lily Nahidi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Exclusive enteral nutrition (EEN) is a well-established approach to the management of Crohn’s disease. Aim. To determine effects of EEN upon inflammation and gut barrier function in a colitis mouse model. Methods. Interleukin-10-deficient mice (IL-10−/−) were inoculated with Helicobacter trogontum and then treated with EEN, metronidazole, hydrocortisone, or EEN and metronidazole combination. Blood and tissue were collected at 2 and 4 weeks with histology, mucosal integrity, tight junction integrity, inflammation, and H. trogontum load evaluated. Results. H. trogontum induced colitis in IL-10−/− mice with histological changes in the cecum and colon. Elevated mucosal IL-8 mRNA in infected mice was associated with intestinal barrier dysfunction indicated by decreased transepithelial electrical resistance and mRNA of tight junction proteins and increased short-circuit current, myosin light chain kinase mRNA, paracellular permeability, and tumor necrosis factor-α and myeloperoxidase plasma levels ( for all comparisons). EEN and metronidazole, but not hydrocortisone, treatments restored barrier function, maintained gut barrier integrity, and reversed inflammatory changes along with reduction of H. trogontum load (versus infected controls ). Conclusion. H. trogontum infection in IL-10−/− mice induced typhlocolitis with intestinal barrier dysfunction. EEN and metronidazole, but not hydrocortisone, modulate barrier dysfunction and reversal of inflammatory changes.