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

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2019-06-06
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Kathrani, Aarti
Lezcano, Victor
Hall, Edward
Jergens, Albert
Seo, Yeon-Jung
Mochel, Jonathan
Atherly, Todd
Allenspach, Karin
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Mochel, Jonathan
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Biomedical Sciences

The Department of Biomedical Sciences aims to provide knowledge of anatomy and physiology in order to understand the mechanisms and treatment of animal diseases. Additionally, it seeks to teach the understanding of drug-action for rational drug-therapy, as well as toxicology, pharmacodynamics, and clinical drug administration.

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The Department of Biomedical Sciences was formed in 1999 as a merger of the Department of Veterinary Anatomy and the Department of Veterinary Physiology and Pharmacology.

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1999–present

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  • College of Veterinary Medicine (parent college)
  • Department of Veterinary Anatomy (predecessor, 1997)
  • Department of Veterinary Physiology and Pharmacology (predecessor, 1997)

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Veterinary Clinical Sciences
The mission of the Veterinary Clinical Sciences Department and the Veterinary Medical Center is to be strong academically, to provide outstanding services, and to conduct research in the multiple areas of Veterinary Clinical Sciences. Our goals are to teach students in the multiple disciplines of Veterinary Clinical Sciences, to provide excellent veterinary services to clients, and to generate and disseminate new knowledge in the areas of Veterinary Clinical Sciences. Our objectives are to provide a curriculum in the various aspects of Veterinary Clinical Sciences which ensures students acquire the skills and knowledge to be successful in their chosen careers. We also strive to maintain a caseload of sufficient size and diversity which insures a broad clinical experience for students, residents, and faculty. In addition, we aim to provide clinical veterinary services of the highest standards to animal owners and to referring veterinarians. And finally, we strive to provide an environment and opportunities which foster and encourage the generation and dissemination of new knowledge in many of the disciplines of Veterinary Clinical Sciences.
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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.

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This article is published as Kathrani, Aarti, Victor Lezcano, Edward J. Hall, Albert E. Jergens, Yeon‐Jung Seo, Jonathan P. Mochel, Todd Atherly, and Karin Allenspach. "Interleukin‐13 and interleukin‐33 mRNA are underexpressed in the duodenal mucosa of German Shepherd dogs with chronic enteropathy." Journal of Veterinary Internal Medicine (2019). DOI: 10.1111/jvim.15544. Posted with permission.

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Tue Jan 01 00:00:00 UTC 2019
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