title: Upregulation of toll-like receptors in chronic enteropathies in dogs.
abstract: 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.
  
  
  OBJECTIVE
  That there is a dysregulation of TLRs recognizing bacterial MAMPs in dogs with IBD.
  
  
  METHODS
  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< or = .017) in expression of TLR2, 4, and 9 between the 6 sampled locations in healthy control dogs (lymph node > small intestine > or = 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
  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.
authors.affiliation: Department of Clinical Veterinary Medicine, Vetsuisse Faculty of the University of Bern, Bern, Switzerland. iwan.burgener@kkh.unibe.ch
authors.forename: I A
authors.initials: IA
authors.lastname: Burgener
authors.forename: A
authors.initials: A
authors.lastname: König
authors.forename: K
authors.initials: K
authors.lastname: Allenspach
authors.forename: S N
authors.initials: SN
authors.lastname: Sauter
authors.forename: J
authors.initials: J
authors.lastname: Boisclair
authors.forename: M G
authors.initials: MG
authors.lastname: Doherr
authors.forename: T W
authors.initials: TW
authors.lastname: Jungi
mesh_terms: D000818:Animals; D016022:Case-Control Studies; D002908:Chronic Disease; D004283:Dog Diseases / Q000235:genetics / Q000378:metabolism*; D004285:Dogs; D005260:Female; D005512:Food Hypersensitivity / Q000235:genetics / Q000378:metabolism / Q000662:veterinary; D041981:Gastrointestinal Tract / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation; D015212:Inflammatory Bowel Diseases / Q000235:genetics / Q000378:metabolism / Q000662:veterinary; D007410:Intestinal Diseases / Q000235:genetics / Q000378:metabolism / Q000662:veterinary*; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D012333:RNA, Messenger; D051193:Toll-Like Receptors