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 withHelicobacter trogontumand 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, andH. trogontumload evaluated.Results.H. trogontuminduced 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-αand myeloperoxidase plasma levels (P<0.01for all comparisons). EEN and metronidazole, but not hydrocortisone, treatments restored barrier function, maintained gut barrier integrity, and reversed inflammatory changes along with reduction ofH. trogontumload (versus infected controlsP<0.05).Conclusion.H. trogontuminfection in IL-10−/−mice induced typhlocolitis with intestinal barrier dysfunction. EEN and metronidazole, but not hydrocortisone, modulate barrier dysfunction and reversal of inflammatory changes.
Disruption of Tight Junction Barrier Function and Upregulation of Inflammatory Signaling Pathway in a Necrotizing Enterocolitis Mouse Model