Peer-reviewed veterinary case report
Measurement of IL-12 (p40, p35), IL-23p19, and IFN-γ mRNA in duodenal biopsies of cats with inflammatory enteropathy.
- Journal:
- Journal of veterinary internal medicine
- Year:
- 2014
- Authors:
- Waly, N E et al.
- Affiliation:
- Department of Animal Medicine
- Species:
- cat
Abstract
BACKGROUND: Dietary hypersensitivity and inflammatory bowel disease (IBD) are important causes of chronic vomiting and diarrhea in cats. IL-23 has been recently found to be a key factor in the immunopathogenesis of IBD in humans but the involvement in IBD has not been investigated in cats. HYPOTHESIS/OBJECTIVES: Expression of genes encoding Il-12p35 and p40, IL-23p19, and IFN-γ may be up-regulated in duodenal biopsy specimens taken from cats with histologic evidence of inflammation. ANIMALS AND METHODS: Duodenal biopsy specimens were collected from control cats (n = 21) and cats with inflammatory enteropathy (n = 13). Routine histopathology, immunohistochemistry (IHC), and qRT-PCR were used to assess expression of MHC class II and to measure gene transcripts encoding the p35, p40, and p19 subunits of the IL-12 family of cytokines and IFN-γ. RESULTS: There were significant differences in expression of mRNA encoding IL-12p35 and IL-23p19 between healthy cats and cats with inflammatory enteropathy. IL-12p35 mRNA was lower in the duodenal mucosa of cats with inflammatory enteropathy compared with the mucosa of healthy cats (P = .001). In contrast, IL-23p19 mRNA expression was higher in duodenal biopsy specimens from cats with inflammatory enteropathy than in those from healthy controls (P = .001). There was no difference in expression of IL-12p40 and IFN-γ mRNA (P > .05). The majority of cats with inflammatory enteropathy had histologic evidence of moderate to severe colitis (score 2). CONCLUSIONS AND CLINICAL IMPORTANCE: The results of this preliminary study suggest that IL-23 plays a role in the pathogenesis of feline inflammatory enteropathy.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/24147775/