Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model
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...
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Online Access: | http://dx.doi.org/10.1155/2013/909613 |
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doaj-dbcea85409f24ddb8b63fa4d5eb523332020-11-24T22:23:38ZengHindawi LimitedBioMed Research International2314-61332314-61412013-01-01201310.1155/2013/909613909613Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse ModelLily Nahidi0Steven T. Leach1Hazel M. Mitchell2Nadeem O. Kaakoush3Daniel A. Lemberg4John S. Munday5Karina Huinao6Andrew S. Day7School of Women’s and Children’s Health, University of New South Wales, Randwick, Sydney, NSW 2031, AustraliaSchool of Women’s and Children’s Health, University of New South Wales, Randwick, Sydney, NSW 2031, AustraliaSchool of Biotechnology and Biomolecular Sciences, University of New South Wales, Randwick, Sydney, NSW 2052, AustraliaSchool of Biotechnology and Biomolecular Sciences, University of New South Wales, Randwick, Sydney, NSW 2052, AustraliaSchool of Women’s and Children’s Health, University of New South Wales, Randwick, Sydney, NSW 2031, AustraliaDepartment of Pathology, Institute of Veterinary, Animal and Biomedical Sciences, Massey University, Palmerston North 4442, New ZealandSchool of Biotechnology and Biomolecular Sciences, University of New South Wales, Randwick, Sydney, NSW 2052, AustraliaSchool of Women’s and Children’s Health, University of New South Wales, Randwick, Sydney, NSW 2031, AustraliaBackground. 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 (P<0.01 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 P<0.05). 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.http://dx.doi.org/10.1155/2013/909613 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lily Nahidi Steven T. Leach Hazel M. Mitchell Nadeem O. Kaakoush Daniel A. Lemberg John S. Munday Karina Huinao Andrew S. Day |
spellingShingle |
Lily Nahidi Steven T. Leach Hazel M. Mitchell Nadeem O. Kaakoush Daniel A. Lemberg John S. Munday Karina Huinao Andrew S. Day Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model BioMed Research International |
author_facet |
Lily Nahidi Steven T. Leach Hazel M. Mitchell Nadeem O. Kaakoush Daniel A. Lemberg John S. Munday Karina Huinao Andrew S. Day |
author_sort |
Lily Nahidi |
title |
Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model |
title_short |
Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model |
title_full |
Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model |
title_fullStr |
Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model |
title_full_unstemmed |
Inflammatory Bowel Disease Therapies and Gut Function in a Colitis Mouse Model |
title_sort |
inflammatory bowel disease therapies and gut function in a colitis mouse model |
publisher |
Hindawi Limited |
series |
BioMed Research International |
issn |
2314-6133 2314-6141 |
publishDate |
2013-01-01 |
description |
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 (P<0.01 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 P<0.05). 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. |
url |
http://dx.doi.org/10.1155/2013/909613 |
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