Research Communications of the 24th ECVIM-CA Congress

No conflicts of interest reported. Canine inflammatory bowel disease (IBD) is an immune-mediated enteropathy likely triggered by environmental and immunoregulatory factors in genetically susceptible dogs. Previous studies suggest a pivotal role for gut bacteria in disease pathogenesis since luminal microbial composition is markedly altered (ie, dysbiosis) at diagnosis. Probiotic bacteria appear to be therapeutically effective in some forms of human IBD. Controlled studies evaluating the efficacy of probiotic therapy for canine IBD have not been previously reported. The aim of the present study was to characterize the mucosa-associated microbiota and determine the clinical, microbiological, and mucosal homeostatic effects of orally administered VSL#3 probiotics in dogs with IBD. Twenty dogs diagnosed with moderate-to-severe IBD (CIBDAI score > 5) were randomized to receive standard therapy (ie, elimination diet and glucocorticoids) with or without probiotic VSL#3. The mucosal microbiota from endoscopic intestinal biopsies of IBD dogs and controls was evaluated by fluorescence in situ hybridization (FISH) targeting the 16S rRNA genes of total bacteria, group-specific organisms, and individual bacterial species shown to be relevant in human IBD. Epithelial tight junction protein (TJP) expression was studied using immunohistochemistry. Clinical signs and changes in mucosal microbiota and TJP expression were assessed before and after probiotic VSL#3 therapy. IBD dogs showed a reduction in GI signs following 8 weeks of probiotic therapy compared with baseline CIBDAI scores (P < 0.05). Adherent and sporadic invasive bacteria (EUB) were observed in the small intestines and colon of healthy dogs. The diseased canine duodenum was nearly bacteria-free. IBD dogs given probiotic VSL #3 had altered spatial redistribution of most bacterial groups in the mucus and adherent compartments of the colon. Subset analysis showed that Lactobacilli were significantly (P < 0.05) increased in the lumen and mucus post-VSL #3, while the number of mucus laden Bifidobacteria approached significance (P = 0.08). Expression of TJP showed that occludin was significantly lower in control intestines as compared to duodenal and colonic mucosa obtained from IBD dogs that received probiotic (P = 0.008 and P = 0.01, respectively). In contrast, claudin-2 expression in the colon was significantly higher (P < 0.002) in control dogs versus VSL #3 treated IBD dogs. Our data demonstrate that probiotic VSL#3 alters some of the mucosa-associated microbiota in dogs with IBD. These probiotic changes in bacterial composition are associated with up-regulated TJP expression indicative of enhanced epithelial barrier integrity, similar to VSL#3-induced disease protection seen in human IBD.