Study on the pathogenesis of canine inflammatory bowel disease: investigation of the intestinal mucosal barrier function and intestinal mucosal cytokine expression.

我们检测了炎症性肠病（IBD）犬十二指肠黏膜紧密连接蛋白和粘附连接蛋白的表达。免疫印迹法检测TJ蛋白（claudin-1、-2、-3、-4、-5、-7和-8）和AJ蛋白（E-cadherin和β -catenin）的表达。结果表明，与健康对照犬相比，IBD犬十二指肠黏膜样品中E-cadherin蛋白的表达明显降低。我们推测T辅助细胞在IBD犬十二指肠黏膜E-cadherin表达变化中起重要作用。因此，我们评估了IBD犬十二指肠黏膜中T细胞亚群（IL-17、ifn - γ、IL-4和IL-10）细胞因子的基因表达。结果表明，各组间各细胞因子mRNA转录水平无显著差异。因此，没有明确的证据表明不同的T辅助细胞因子参与犬IBD的发病机制。

We examined the expression of tight junction and adherens junction protein in duodenal mucosa sample of dogs with inflammatory bowel disease (IBD). The expression of TJ proteins (claudin-1, -2, -3, -4, -5, -7 and -8), and AJ proteins (E-cadherin and beta-catenin) were determined by means of immunoblotting. As a result, expression of E-cadherin protein was significantly lower in duodenal mucosa samples of dogs with IBD than it was in samples obtained from healthy control dogs. We speculated that T helper cells have important roles in change in expression of E-cadherin in duodenal mucosa of IBD dogs. Thus, we evaluated the gene expression of cytokines of T cell subsets (IL-17, IFN-gamma, IL-4, and IL-10) in duodenal mucosa from dogs with IBD. As a result, there was no significant difference in each cytokine mRNA transcription level between groups. Thus, there is no clear evidence for the involvement of distinct T helper cytokine in the pathogenesis of canine IBD.