Canine and feline inflammatory bowel disease (IBD) denotes a heterogeneous group of idiopathic, chronic, relapsing inflammatory disorders of the gastrointestinal tract that are immunologically-mediated. While their exact etiologies remain unknown, results from basic science and clinical studies suggest that interplay between genetic factors and enteric bacteria are crucial for disease development, owing to abnormal host responses directed against the commensal microbiota. Key clinical signs include vomiting, diarrhea and weight loss, and histopathologic lesions of inflammation may involve the stomach, small intestine, or colon. Recent advances in molecular tools, disease activity indices, and biomarker development now permit objective assessment of IBD severity at diagnosis and in response to various therapies. Treatment of IBD involves both dietary and pharamacologic interventions as well as therapeutic manipulation of the enteric microbiota through the use of antibiotics and soluble fiber (prebiotic) supplements. Here we provide a comprehensive overview on the etiopathogenesis, clinical features, diagnosis strategies, current treatment recommendations, and outcomes from veterinary studies in dogs and cats with IBD. We also offer scientific comparison between human and canine IBD.
"Canine IBD denotes a group of idiopathic, chronic, relapsing inflammatory disorders of the gastrointestinal tract that are immunologically-mediated (Allenspach et al., 2007; Jergens and Simpson, 2012). The pathogenesis of IBD in dogs is complex and likely involves defects in mucosal barrier function and mucosal immunity, similar to human IBD (Allenspach, 2011). "
[Show abstract][Hide abstract] ABSTRACT: Canine idiopathic inflammatory bowel disease (IBD) is believed to result from complex interplay between genetic, microbial, and immunologic factors. Abnormal cell death by apoptosis may result in the persistence of activated intestinal T cells that contribute to mucosal inflammation and clinical severity. To test this hypothesis, we investigated the mucosal expression of pro- and anti-apoptotic proteins in different intestinal compartments and their association with inflammatory indices in dogs with IBD. Apoptosis of lamina propria (LP) T cells in duodenal, ileal, and colonic tissues in control and IBD dogs was analyzed by caspase 3/Bcl-2 immunohistochemistry and TUNEL assays. Densities and distributions of LP caspase 3 and Bcl-2 cells were correlated to histopathologic lesions and the clinical activity index (CIBDAI). Compared to control tissues, IBD dogs had significantly (P<0.01) fewer caspase 3 cells in colonic mucosa. Double immunostaining identified the majority of apoptotic cells as TUNEL+/caspase 3+. Within intestinal mucosa of IBD dogs, there were significantly greater numbers of Bcl-2 cells at the apical and basilar villus in the duodenum as compared to the colon and to the apical and basilar villus in the ileum (P<0.001 for all comparisons). There were significantly greater numbers of Bcl-2 cells at the apical and basilar villus of the duodenum but significantly fewer numbers of Bcl-2 cells at the apical villus of the ileum in IBD dogs compared with controls (P<0.001, P<0.001, and P<0.02, respectively). There was a significant association between the number of Bcl-2 cells in the duodenum of IBD dogs and the CIBDAI (P<0.001 each for mild, moderate and severe clinical IBD). In conclusion, apoptosis of T lymphocytes varies within intestinal compartments of dogs with IBD. Mucosal imbalance of Bcl-2/caspase 3 expression favors T cell resistance to apoptosis which may contribute to T cell accumulation and chronic intestinal inflammation, similar to human IBD.
"Canine inflammatory bowel disease (IBD) is a diversified group of intestinal disorders characterized by cellular infiltration of the mucous membrane in the lamina propria area (Craven et al. 2004, Allenspach et al. 2006, Allenspach et al. 2007, Jergens and Simpson 2012). In gastroenterology centers, canine inflammatory bowel disease is diagnosed in view of the results of histopathological examinations of the intestinal mucous membrane and by ruling out other known Correspondence to: A. Rychlik, e-mail: email@example.com "
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to assess the degree of correlation between the intensity of clinical symptoms and the macroscopic and histopathological evaluation of the small intestinal mucous membrane in dogs. The results point to a statistically significant correlation between the values of the CIBDAI index and the histopathological assessment of the duodenum mucous membrane in patients with minor and moderate intensity of the disease. The lowest correlation coefficient was obtained for the indicator comparing macroscopic and histopathological evaluations. A positive correlation between the CIBDAI score and the histopathological index offers a base for applying it in the monitoring and treatment of mild, moderate and severe cases of canine inflammatory bowel disease.
[Show abstract][Hide abstract] ABSTRACT: Canine inflammatory bowel disease is a group of chronic enteropathies characterized by persistent or recurring gastric symptoms with an unknown etiology which are related to histopathological changes in the mucosa of the small and large bowel in the form of cellular infiltration in the mucosal lamina propria. Recent years have witnessed a growing number of investigations into the role of the immune system and, in particular, cytokines in the development of IBD. In this article, the expression of pro-inflammatory (IL-1, IL-2, IL-5, IL-6, IL-12, IL-18, IFN-gamma, TNF-alpha) and anti-inflammatory cytokines (IL-4, IL-10) was compared in canine patients with IBD based on clinical presentation, breed, lamina propria cell infiltrate and histopathological grade. Only selected studies confirmed higher mRNA expression levels of cytokines IL-2, IL-4, IL-5, IL-12p40, IFN-gamma, TNF-alpha and TGF-beta in dogs with IBD in comparison with healthy subjects. GSD were strongly represented in most study populations. Dogs with LPE were characterized by elevated levels of IL-1alpha, IL-1beta, IL-2, IL-5, IL-6, IL-12, TNF-alpha, TGF-beta. The present studies of canine patients with LPC revealed the mRNA expression of cytokines IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12p35, IL-12p40, IFN-gamma, TNF-alpha, TGF-beta. In the reviewed studies, the progression of IBD was not accompanied by changes in the mRNA express-
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