Aquaculture Protein Centre (a Centre of Excellence), Department of Basic Sciences and Aquatic Medicine, Norwegian School of Veterinary Science, P.O. Box 8146 Dep., 0033 Oslo, Norway.
Cytokine. 2012 Oct;60(1):186-96. doi: 10.1016/j.cyto.2012.05.027. Epub 2012 Jul 12.
Progression of soybean meal (SBM)-induced enteropathy in Atlantic salmon (Salmo salar L.) distal intestine (DI) was studied to investigate pathophysiological mechanisms and immune responses. Seawater-adapted salmon were fed an extracted SBM-containing diet (200 g kg(-1)) from day 1-21 and compared with fish fed a fishmeal-based diet (day 0). Histological evaluation of the DI revealed signs of inflammation from day 5, which progressively increased in severity and affected more fish with increasing SBM exposure time. The expression profiles of 16 genes were analyzed by quantitative PCR. The pro-inflammatory cytokines interleukin 17A (IL-17A), IL-1β, interferon α (IFNα) and IFNγ, as well as IL-17A receptor, T-cell receptor γ (TCRγ), cluster of differentiation 4α (CD4α), CD8β, transforming growth factor β (TGFβ), trypsin, protease-activated receptor 2 (PAR2) and myeloid differentiation primary response gene 88 (MyD88) were significantly up-regulated during early and/or late inflammation stages, whereas interferon-γ-inducible lysosomal thiol reductase (GILT) was downregulated. Up-regulation of TCRγ from day seven suggests proliferation of intraepithelial γδ T cells. IL-17A, up-regulated by 218-fold during early inflammation, indicates involvement of T helper 17 cells in the pathogenesis of the SBM-induced inflammatory response.
研究了大豆粕(SBM)诱导大西洋鲑(Salmo salar L.)远端肠(DI)肠病的进展,以研究其病理生理机制和免疫反应。从第 1-21 天,适应海水的鲑鱼被喂食含有提取的 SBM 的饮食(200 g kg(-1)),并与喂食基于鱼粉的饮食(第 0 天)的鱼进行比较。DI 的组织学评估显示,从第 5 天开始出现炎症迹象,随着 SBM 暴露时间的增加,炎症的严重程度逐渐增加,受影响的鱼也越来越多。通过定量 PCR 分析了 16 个基因的表达谱。促炎细胞因子白细胞介素 17A(IL-17A)、IL-1β、干扰素 α(IFNα)和 IFNγ,以及 IL-17A 受体、T 细胞受体 γ(TCRγ)、分化簇 4α(CD4α)、CD8β、转化生长因子 β(TGFβ)、胰蛋白酶、蛋白酶激活受体 2(PAR2)和髓样分化初级反应基因 88(MyD88)在早期和/或晚期炎症阶段显著上调,而干扰素-γ诱导的溶酶体硫醇还原酶(GILT)下调。第 7 天 TCRγ 的上调表明上皮内 γδ T 细胞的增殖。早期炎症期间上调 218 倍的 IL-17A 表明辅助性 T 细胞 17 细胞参与了 SBM 诱导的炎症反应的发病机制。