Expression of genes encoding interleukin 15 and its receptor subunits in the duodenal and colonic mucosae of dogs with chronic enteropathy

Furukawa, Rintaro; Hara, Yuna; Furuya, Keiko; Takahashi, Kaho; Nishimura, Rinka; Shingaki, Tomoaki; Osada, Hironari; Kondo, Hirotaka; Ohmori, Kitaro

doi:10.1016/j.vas.2022.100256

Cited by 1 publication

(1 citation statement)

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“…However, the involvement of IL-15 in the pathogenesis of canine CE was not found in the present study or in a previous study. 16 Gliadin-independent mechanisms or physiological effects of gliadin that differ from those in humans may be involved in the pathogenesis of canine CE. However, it is important to note that cytokine expression patterns in celiac disease vary according to the clinical stage of the disease.…”

Section: Discussionmentioning

confidence: 99%

Pro-inflammatory cytokine expression and the STAT1/3 pathway in canine chronic enteropathy and intestinal T-cell lymphoma

Kojima,

Chambers,

Nakashima

et al. 2023

Vet Pathol

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The accumulation of intraepithelial lymphocytes (IELs) is a histopathological feature of canine chronic enteropathy (CE), and IELs are considered the cells of origin of intestinal T-cell lymphoma (ITCL). However, the pathogenic mechanism of IEL activation in CE remains unclear. This study hypothesized that the expression of proinflammatory cytokines, associated with cytotoxic T/NK-cell activation, is upregulated in CE and ITCL, and examined the expression of IFN-γ, IL-2, IL-12p35, IL-12p40, IL-15, and IL-21 and the downstream signal transducers and activators of transcription (STAT) pathway in the duodenal mucosa of dogs without lesions ( n = 11; NC), with IEL–CE ( n = 19; CE without intraepithelial lymphocytosis), IEL+CE ( n = 29; CE with intraepithelial lymphocytosis), and with ITCL ( n = 60). Quantitative polymerase chain reaction (PCR) revealed that IFN-γ and IL-21 were higher in IEL+CE than in IEL–CE or NC. Western blot revealed upregulation of STAT1 and STAT3 in IEL+CE. Double-labeling immunohistochemistry revealed a positive correlation between the Ki67 index of CD3+ T-cells and IFN-γ expression levels. Immunohistochemistry revealed a higher ratio of p-STAT1-positive villi in IEL+CE and ITCL than IEL–CE and NC, which positively correlated with IFN-γ expression levels. Among the 60 ITCL cases, neoplastic lymphocytes were immunopositive for p-STAT1 in 28 cases and p-STAT3 in 29 cases. These results suggest that IFN-γ and IL-21 contribute to the pathogenesis of IEL+CE, and IFN-γ may be involved in T-cell activation and mucosal injury in CE. STAT1 and STAT3 activation in ITCL cells suggests a role for the upregulation of the STAT pathway in the pathogenesis of ITCL.

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Section: Discussionmentioning

confidence: 99%