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Interleukin‐13 and interleukin‐33 mRNA are underexpressed in the duodenal mucosa of German Shepherd dogs with chronic enteropathy

Author:
Kathrani, Aarti, Lezcano, Victor, Hall, Edward J., Jergens, Albert E., Seo, Yeon‐Jung, Mochel, Jonathan P., Atherly, Todd, Allenspach, Karin
Source:
Journal of veterinary internal medicine 2019 v.33 no.4 pp. 1660-1668
ISSN:
0891-6640
Subject:
Beagle, German Shepherd, biopsy, colitis, dogs, gene expression, genes, genome-wide association study, humans, in situ hybridization, interleukin-13, messenger RNA, pathogenesis, patients, retrospective studies, villi
Abstract:
BACKGROUND: A recent genome‐wide association study in German Shepherd dogs (GSDs) with chronic enteropathy (CE) has identified polymorphisms in the Th2 cytokine genes. HYPOTHESIS/OBJECTIVE: To determine if the expression of the Th2 cytokines, interleukin‐13 (IL‐13) and interleukin‐33 (IL‐33), is altered in the duodenal mucosa of GSDs with CE compared to non‐GSDs with CE and healthy dogs. ANIMALS: Twenty client‐owned dogs diagnosed with CE (10 GSDs and 10 non‐GSDs) at the Bristol Veterinary School and 8 healthy Beagle dogs from the Iowa State University Service Colony. METHODS: Retrospective study using archived paraffin‐embedded duodenal biopsy samples. A novel RNA in situ hybridization technology (RNAscope) was used to hybridize IL‐13 and IL‐33 mRNA probes onto at least 10 sections from duodenal biopsy samples for each dog. RNAscope signals were visualized using a microscope and semi‐quantitative assessment was performed by a single operator. RESULTS: Based on duodenal villus, subvillus, epithelial, and lamina propria average expression scores, GSDs with CE had significantly lower IL‐13 and IL‐33 mRNA expression compared to non‐GSDs with CE (IL‐13, P < .04; IL‐33, P < .02) and healthy Beagle dogs (IL‐13, P < .02; IL‐33, P < .004). CONCLUSIONS AND CLINICAL IMPORTANCE: Similar to human patients with ulcerative colitis, a subtype of human inflammatory bowel disease, these data indicate that Th2 cytokines may be involved in the pathogenesis of CE in GSDs.
Agid:
6541407