Biomarkers in canine inflammatory bowel disease diagnostics

Abstract

Canine inflammatory bowel disease (IBD) is a heterogeneous group of chronic gastrointestinal disorders. The etiology, similar to human IBD, remains unknown. Canine IBD is diagnosed by exclusion, which is a long, time and money-consuming process due to the need of elimination of other diseases presenting with similar symptoms. Therefore, a search for a specific and sensitive marker is needed to overcome these difficulties.The article is divided into 3 sections presenting up-to-date information about laboratory markers, immunohistochemical markers and changes in the neurochemical coding of the enteric nervous system, concentrating on their usefulness and future applications. Data concerning laboratory and immunohistochemical markers is based mainly on canine IBD, while the neuroimmunohistochemistry section presents knowledge from human IBD due to the lack of such studies in veterinary medicine.

Spontaneous and transgenic rodent models of inflammatory bowel disease

“…Clinical inflammatory bowel disease syndromes include Ulcerative Colitis (UC) in which limited mucosal and submucosal inflammatory processes predominantly affect the colon and adjacent areas of the rectum, and Crohn's Disease (CD) characterized by chronic intermittent relapsing discontinuous transmural inflammation of the bowel with intestinal and perianal fistulation [ 9 ]. Spontaneous natural IBD is also found in dogs and cats, horses and primates [ 10 11 ]. Canine phenotypic IBD disease classifications include lymphoplasmacytic enteritis, eosinophilic gastroenteritis, eosinophilic colitis, granulomatous colitis and histiocytic ulcerative colitis and neuronal hyperplasia [ 10 11 12 13 14 ].…”

“…Spontaneous natural IBD is also found in dogs and cats, horses and primates [ 10 11 ]. Canine phenotypic IBD disease classifications include lymphoplasmacytic enteritis, eosinophilic gastroenteritis, eosinophilic colitis, granulomatous colitis and histiocytic ulcerative colitis and neuronal hyperplasia [ 10 11 12 13 14 ]. In horses, IBD is usually expressed as weight loss and clinical colitis which exhibit variable long-term responses to corticosteroid and anthelmintic treatment [ 15 ].…”

“…While many histological disease phenotypes and lesions expressed by human and animal patients are similar, some do differ, with the result that there is no one animal model that replicates every major expression of human or animal IBD among experimental animal models. Additionally, in some instances functional phenotypes and histologic indications of inflammatory bowel disease can resemble other disease entities, which confound study and clinical diagnosis, and must be identified, treated and/or eliminated from consideration in determining disease etiology and pathogenesis [ 2 3 5 10 11 12 13 18 ].…”

“…Patients have traditionally been diagnosed and categorized based on endoscopic histopathological lesion appearance and clinical responsiveness to medication [ 2 3 5 13 18 19 ]. There are several different systems that have been used to characterize histological lesions observed in IBD, but classical histological interpretation of mixed inflammatory cellular infiltrates can be very subjective due to their occurrence in response to non-IBD related disease etiologies, and also because a uniform set of prognostic biomarkers has not yet been fully developed in human or veterinary medicine for CD or UC diagnosis [ 3 11 ]. Most small animal IBD patients are initially treated with diet restrictions, use of metronidazole to change the intestinal microbiota by eliminating anaerobic bacterial species; increased fiber content and anti-inflammatory products [ 12 20 ].…”

“…However, many of these drug and biological adjuvant regiments do have significant side effects, and it would be advantageous to identify predictive biomarkers and new, effective therapeutic protocols to assist in managing these diseases [ 10 11 21 ]. Identifying biomarkers associated with different pathogenic and/or progressive stages in inflammatory bowel disease in humans has been difficult in part because of great variability in the contribution of underlying mechanisms to disease incidence, and in disease onset, progression, and remission over time [ 21 ].…”