Wang Kai, Dong Hao, Qi Yu, Pei Zhihua, Yi Shushuai, Yang Xiaojie, Zhao Yanli, Meng Fanxing, Yu Shouping, Zhou Tiezhong, Hu Guixue
College of Animal Science and Technology (Wang, Qi, Pei, Yi, Yang, Zhao, Meng, Yu, Hu); College of Life Science, Jilin Agricultural University, Xincheng Street No. 2888, Changchun (Dong); College of Animal Husbandry & Veterinary, Jinzhou Medical University, Renmin Street, No. 48, Section 5, Jinzhou 121001, China (Zhou).
Can J Vet Res. 2017 Apr;81(2):122-128.
In order to study the ability of to ameliorate murine enteritis, 18 mice were randomly divided into 3 groups: the enteritis group, intervention group, and control group. The interleukin (IL)-6 and transforming growth factor-β (TGF)-β content in mouse peripheral blood and duodenum was detected using an enzyme-linked immunosorbent assay (ELISA). The number of CD4CD25Foxp3 T-regulatory cells (Tregs) and CD4IL-17A Th17 cells in the mesenteric lymph nodes (MLN) and spleen were detected using flow cytometry, and quantitative reverse transcription polymerase chain reaction (PCR) and western blot analysis were used to measure Foxp3 and retinoid-related orphan receptor-γ (RORγt) mRNA and protein expression in the MLN. Histological changes in the duodenum were observed. Results indicate that in the intervention group, IL-6 content in mouse peripheral blood and duodenum was significantly lower than in the enteritis group ( < 0.05), while TGF-β content was significantly increased compared to the enteritis group ( < 0.05). For the intervention group, the percentages of CD4CD25Foxp3 Tregs in spleen and MLN were increased ( < 0.05), while the percentages of CD4IL-17A Th17 cells were decreased compared to the enteritis group ( < 0.05). The expression of Foxp3 mRNA and protein in the intervention group was higher than in the enteritis group, while RORγt mRNA and protein were significantly lower ( < 0.05). After mice in the enteritis group were treated with duodenal inflammation was relieved. This study demonstrated that could have possible implications for the enterotoxigenic (ETEC) induced intestinal inflammation by regulating the ratio imbalance of Th17/Treg cells.
为研究[具体物质]改善小鼠肠炎的能力，将18只小鼠随机分为3组：肠炎组、干预组和对照组。采用酶联免疫吸附测定（ELISA）检测小鼠外周血和十二指肠中白细胞介素（IL）-6和转化生长因子-β（TGF）-β的含量。使用流式细胞术检测肠系膜淋巴结（MLN）和脾脏中CD4CD25Foxp3调节性T细胞（Tregs）和CD4IL-17A辅助性T细胞17（Th17）的数量，并采用定量逆转录聚合酶链反应（PCR）和蛋白质印迹分析来测定MLN中Foxp3和视黄酸相关孤儿受体-γ（RORγt）的mRNA和蛋白表达。观察十二指肠的组织学变化。结果表明，干预组小鼠外周血和十二指肠中的IL-6含量显著低于肠炎组（P<0.05），而TGF-β含量与肠炎组相比显著升高（P<0.05）。对于干预组，脾脏和MLN中CD4CD25Foxp3 Tregs的百分比增加（P<0.05），而与肠炎组相比，CD4IL-17A Th17细胞的百分比降低（P<0.05）。干预组中Foxp3 mRNA和蛋白的表达高于肠炎组，而RORγt mRNA和蛋白则显著降低（P<0.05）。肠炎组小鼠经[具体物质]治疗后，十二指肠炎症得到缓解。本研究表明，[具体物质]可能通过调节Th17/Treg细胞的比例失衡对产肠毒素大肠杆菌（ETEC）诱导的肠道炎症产生影响。
