Upregulation of signal transducer and activator of transcription 3 in dogs with chronic inflammatory enteropathies.


Journal

Journal of veterinary internal medicine
ISSN: 1939-1676
Titre abrégé: J Vet Intern Med
Pays: United States
ID NLM: 8708660

Informations de publication

Date de publication:
May 2021
Historique:
revised: 11 04 2021
received: 25 11 2020
accepted: 16 04 2021
pubmed: 7 5 2021
medline: 29 6 2021
entrez: 6 5 2021
Statut: ppublish

Résumé

In inflammatory bowel disease (IBD) in humans, phosphorylated signal transducer and activator of transcription 3 (pSTAT3) is upregulated in mucosal epithelial cells and correlates with clinical severity. To investigate the expression pattern of pSTAT3 in the mucosa of dogs with chronic inflammatory enteropathy (CIE) and explore correlations between its expression and clinical and histopathological severity scoring. Twenty-eight canine CIE patients grouped into food-responsive enteropathy (FRE;  9), steroid-responsive enteropathy (SRE;  10), and protein-losing enteropathy (PLE;  9). Ten healthy beagle dogs served as controls (CO). Retrospective case control study. Immunohistochemistry was used to detect pSTAT3 in canine duodenal mucosa samples. Compared to CO, SRE (P < .001) and PLE (P < .001) dogs had significantly higher pSTAT3 expression in the villus epithelium. The SRE group had a significantly higher expression in the villus lamina propria (VLP) compared to controls (P = .009). In the crypt epithelium (CE), all CIE dogs had significantly higher pSTAT3 expression (FRE, P = .002; SRE, P = .003; PLE, P < .001) compared to CO. In the lamina propria crypt region (CLP), dogs with FRE (P = .04) and SRE (P = .03) had significantly upregulated pSTAT3 compared to controls. A positive correlation was found between canine chronic enteropathy clinical activity index (CCECAI) scoring and pSTAT3 expression for both epithelial (rho = .541; P < .001) and crypt regions (rho = .32; P = .02). pSTAT3 is upregulated in CIE in dogs, correlates with clinical severity, and may be helpful as a clinical marker in dogs with CIE.

Sections du résumé

BACKGROUND BACKGROUND
In inflammatory bowel disease (IBD) in humans, phosphorylated signal transducer and activator of transcription 3 (pSTAT3) is upregulated in mucosal epithelial cells and correlates with clinical severity.
HYPOTHESIS/OBJECTIVE OBJECTIVE
To investigate the expression pattern of pSTAT3 in the mucosa of dogs with chronic inflammatory enteropathy (CIE) and explore correlations between its expression and clinical and histopathological severity scoring.
ANIMALS METHODS
Twenty-eight canine CIE patients grouped into food-responsive enteropathy (FRE;  9), steroid-responsive enteropathy (SRE;  10), and protein-losing enteropathy (PLE;  9). Ten healthy beagle dogs served as controls (CO).
METHODS METHODS
Retrospective case control study. Immunohistochemistry was used to detect pSTAT3 in canine duodenal mucosa samples.
RESULTS RESULTS
Compared to CO, SRE (P < .001) and PLE (P < .001) dogs had significantly higher pSTAT3 expression in the villus epithelium. The SRE group had a significantly higher expression in the villus lamina propria (VLP) compared to controls (P = .009). In the crypt epithelium (CE), all CIE dogs had significantly higher pSTAT3 expression (FRE, P = .002; SRE, P = .003; PLE, P < .001) compared to CO. In the lamina propria crypt region (CLP), dogs with FRE (P = .04) and SRE (P = .03) had significantly upregulated pSTAT3 compared to controls. A positive correlation was found between canine chronic enteropathy clinical activity index (CCECAI) scoring and pSTAT3 expression for both epithelial (rho = .541; P < .001) and crypt regions (rho = .32; P = .02).
CONCLUSIONS AND CLINICAL IMPORTANCE CONCLUSIONS
pSTAT3 is upregulated in CIE in dogs, correlates with clinical severity, and may be helpful as a clinical marker in dogs with CIE.

Identifiants

pubmed: 33955083
doi: 10.1111/jvim.16141
pmc: PMC8163116
doi:

Substances chimiques

STAT3 Transcription Factor 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1288-1296

Informations de copyright

© 2021 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.

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Auteurs

Anita Manz (A)

Internal Medicine, Clinic for Small Animals, Department for Companion Animals and Horses, University of Veterinary Medicine, Vienna, Austria.

Karin Allenspach (K)

Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA.

Stefan Kummer (S)

Department for Pathobiology, University of Veterinary Medicine, Vienna, Austria.

Barbara Richter (B)

Institute of Pathology, University of Veterinary Medicine, Vienna, Austria.

Ingrid Walter (I)

VetCore Facility for Research, University of Veterinary Medicine, Vienna, Austria.

Sabine Macho-Maschler (S)

Institute of Animal Breeding and Genetics, University of Veterinary Medicine, Vienna, Austria.
Department of Biomedical Sciences, Unit of Physiology, Pathophysiology and Experimental Endocrinology, University of Veterinary Medicine, Vienna, Austria.

Alexander Tichy (A)

Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria.

Iwan A Burgener (IA)

Internal Medicine, Clinic for Small Animals, Department for Companion Animals and Horses, University of Veterinary Medicine, Vienna, Austria.

Nicole Luckschander-Zeller (N)

Internal Medicine, Clinic for Small Animals, Department for Companion Animals and Horses, University of Veterinary Medicine, Vienna, Austria.

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