Immunohistochemical Findings in Idiopathic Inflammatory Bowel Disease in Nine Cats

Inflammatory bowel disease is a term referring to a clinical condition characterized by recurrent/persistent gastrointestinal signs, which cannot be diagnosed only through histological findings, being an elimination diagnosis and needing therefore the previous exclusion of all other possible causes of gastrointestinal signs. The aim of the present study was to compare the expression of different cytokines on endoscopic biopsy samples of the small and large intestine of cats suffering from inflammatory bowel disease and healthy controls, by immunohistochemistry evaluation. Nine cats referred for chronic gastrointestinal signs to the Gastroenterology Service, Teaching Hospital, Faculty of Veterinary Sciences, University of Buenos Aires, were included. After being administered with antiparasitic drugs and after running complete laboratory exams, abdominal ultrasonography, etc., upper and lower gastrointestinal endoscopy with biopsy samplings for histopathology and immunohistochemistry was then performed. Controls were represented by archived samples from healthy cats (University of Camerino, Italy, Veterinary Pathology Unit Archive). On biopsy samples, the immunohistochemistry expression of the following antibodies was evaluated: TGF-beta, CD3(+), FoxP3(+), TNF-alpha, IL-1 beta, IL-10, IL-12, and Th-17(+). Statistic analysis was performed with the nonparametric Mann-Whitney test and with Spearman test, considering significant p0.05. TNF-alpha, IL-1 beta, IL-12, and CD3(+) were significantly differently expressed between cats suffering from inflammatory bowel disease and controls, while no differences were found regarding TGF-beta, IL-10, and FOXP3. A positive correlation was also found between proinflammatory cytokines and proinflammatory cytokines plus lymphocytes that were at the same time related to IL-10 and TGF-beta. On the other hand, a negative correlation was found between proinflammatory and regulatory cytokines. Our results suggest an imbalance in the immune response which may play a role in the etiopathogenesis of feline inflammatory bowel disease.