Upregulation of toll-like receptors in chronic enteropathies in dogs

Burgener, I A; König, A; Allenspach, K; Sauter, S N; Boisclair, J; Doherr, M G; Jungi, T W (2008). Upregulation of toll-like receptors in chronic enteropathies in dogs. Journal of veterinary internal medicine, 22(3), pp. 553-60. Oxford: Wiley-Blackwell 10.1111/j.1939-1676.2008.0093.x

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Background: Inflammatory bowel disease (IBD) is thought to result from a dysregulated interaction between the host immune system and commensal microflora. Toll-like receptors (TLRs) recognize microbe-associated molecular patterns (MAMPs), but their role in enteropathies in dogs is unknown. Hypothesis: That there is a dysregulation of TLRs recognizing bacterial MAMPs in dogs with IBD. Animals: Sixteen healthy beagles and 12 dogs with steroid-treated (ST) and 23 dogs with food-responsive (FR) diarrhea. Methods: Prospective, observational study. mRNA expression of canine TLR2, 4, and 9 was evaluated by quantitative real-time RT-PCR in duodenal and colonic biopsies obtained before and after standard therapy. Samples from control dogs were taken at necropsy, with additional biopsies of stomach, jejunum, ileum, and mesenteric lymph node in 6 dogs. Results: There were significant differences (P</= .017) in expression of TLR2, 4, and 9 between the 6 sampled locations in healthy control dogs (lymph node > small intestine >/= colon). Before therapy, ST expressed more mRNA than control dogs for all 3 receptors (P < .05). There were no significant differences between pretreatment and posttreatment values, even though 32/35 dogs improved clinically. No associations were found when comparing receptor mRNA expression with either histology or clinical activity scores. Conclusions and Clinical Importance: Bacteria-responsive TLR2, 4, and 9 are upregulated in duodenal and colonic mucosa in IBD. This might lead to increased inflammation through interaction with the commensal flora. The absence of significant changes after therapy despite clinical improvement might point toward the existence of a genetic predisposition to IBD as described in human IBD.

Item Type:	Journal Article (Original Article)
Division/Institute:	05 Veterinary Medicine > Department of Clinical Veterinary Medicine (DKV) > DVK - Clinical Research [discontinued] 05 Veterinary Medicine > Department of Clinical Veterinary Medicine (DKV) > Small Animal Clinic 05 Veterinary Medicine > Department of Clinical Research and Veterinary Public Health (DCR-VPH) > Experimental Clinical Research 05 Veterinary Medicine > Department of Infectious Diseases and Pathobiology (DIP) > Institute of Virology and Immunology
UniBE Contributor:	Burgener, Iwan, König, Annemarie, Allenspach, K., Doherr, Marcus, Jungi, Thomas
ISSN:	0891-6640
Publisher:	Wiley-Blackwell
Submitter:	Factscience Import
Date Deposited:	04 Oct 2013 15:00
Last Modified:	05 Dec 2022 14:18
Publisher DOI:	10.1111/j.1939-1676.2008.0093.x
PubMed ID:	18466244
Web of Science ID:	000255908300006
URI:	https://boris.unibe.ch/id/eprint/26047 (FactScience: 63363)