Journal
VETERINARY AND ANIMAL SCIENCE
Volume 17, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.vas.2022.100256
Keywords
Chronic enteropathy; Dog; Inflammatory bowel disease; Interleukin-15
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This study investigated the role of IL-15 signaling in canine chronic enteropathy (CE). The findings suggest that decreased expression of IL-15R alpha might be involved in the pathogenesis of duodenitis in dogs with immunosuppressant-responsive enteropathy (IRE). Furthermore, IL-15 signaling appears to play different roles in duodenitis and colitis in dogs with different subtypes of CE. However, there were no correlations between the gene expression levels of IL-15R alpha and disease severity in the duodenum of dogs with IRE. Further studies are necessary to investigate the localization of IL-15R alpha protein and how impaired IL-15R alpha expression contributes to duodenitis in dogs with IRE.
A pro-inflammatory role of interleukin (IL)-15 and IL-15 receptor (R) in chronic intestinal inflammation, such as inflammatory bowel disease, has been reported in humans. However, the contribution of IL-15 signaling in the pathogenesis of canine chronic enteropathy (CE) remains unclear. Therefore, as a first step in elucidating the importance of IL-15 signaling in canine CE, we measured the mRNA expression of IL-15 and IL-15R subunits, including IL-15R alpha, IL-15R beta, and IL-15R gamma, in the duodenal and colonic mucosae of healthy dogs and those with CE, including food-responsive enteropathy (FRE), antibiotic-responsive enteropathy (ARE), and immunosuppressant-responsive enteropathy (IRE). Real-time PCR analysis revealed significantly lower IL-15R alpha mRNA expression levels in the duodenal mucosa of dogs with IRE compared to healthy dogs. In contrast, the mRNA expression levels of IL-15, IL-15R beta, and IL-15R gamma in the duodenal mucosa and IL-15, IL-15R alpha, IL-15R beta, and IL-15R gamma in the colonic mucosa did not differ among healthy dogs and those with FRE, ARE, or IRE. These findings suggest that decreased mRNA expression of IL-15R alpha might be involved in the pathogenesis of duodenitis in dogs with IRE. Moreover, even in canine CE, IL-15 signaling appears to play different roles in duodenitis and colitis in dogs with FRE, ARE, and IRE. However, there were no correlations between the gene expression levels of IL-15R alpha and clinical severity or histopathological scores in the duodenum of dogs with IRE. Further studies are necessary to investigate the IL-15R alpha protein localization and to determine how impaired IL-15R alpha expression contributes to the development of duodenitis in dogs with IRE.
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