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Microarray analysis reveals the inhibition of intestinal expression of nutrient transporters in piglets infected with porcine epidemic diarrhea virus

机译:微阵列分析显示抑制猪瘟疫腹泻病毒感染仔猪营养转运蛋白营养转运蛋白的抑制作用

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Porcine epidemic diarrhea virus (PEDV) infection can induce intestinal dysfunction, resulting in severe diarrhea and even death, but the mode of action underlying these viral effects remains unclear. This study determined the effects of PEDV infection on intestinal absorption and the expression of genes for nutrient transporters via biochemical tests and microarray analysis. Sixteen 7-day-old healthy piglets fed a milk replacer were randomly allocated to one of two groups. After 5-day adaption, piglets (n?=?8/group) were orally administrated with either sterile saline or PEDV (the strain from Yunnan province) at 10sup4.5/sup TCIDsub50/sub (50% tissue culture infectious dose) per pig. All pigs were orally infused D-xylose (0.1?g/kg BW) on day 5 post PEDV or saline administration. One hour later, jugular vein blood samples as well as intestinal samples were collected for further analysis. In comparison with the control group, PEDV infection increased diarrhea incidence, blood diamine oxidase activity, and iFABP level, while reducing growth and plasma D-xylose concentration in piglets. Moreover, PEDV infection altered plasma and jejunal amino acid profiles, and decreased the expression of aquaporins and amino acid transporters (L-type amino acid transporter 1, sodium-independent amino acid transporter, B(°sup,+/sup)-type amino acid transport protein, sodium-dependent neutral amino acid transporter 1, sodium-dependent glutamate/aspartate transporter 3, and peptide transporter (1), lipid transport and metabolism-related genes (lipoprotein lipase, apolipoprotein A1, apolipoprotein A4, apolipoprotein C2, solute carrier family 27 member 2, solute carrier family 27 member 4, fatty acid synthase, and long-chain acyl-CoA synthetase (3), and glucose transport genes (glucose transporter-2 and insulin receptor) in the jejunum. However, PEDV administration increased mRNA levels for phosphoenolpyruvate carboxykinase 1, argininosuccinate synthase 1, sodium/glucose co-transporter-1, and cystic fibrosis transmembrane conductance regulator in the jejunum. Collectively, these comprehensive results indicate that PEDV infection induces intestinal injury and inhibits the expression of genes encoding for nutrient transporters.
机译:猪流行性腹泻病毒(PEDV)感染可诱导肠功能障碍,导致严重的腹泻甚至死亡,但这些病毒效应的行动模式仍然尚不清楚。该研究确定了PEDV感染通过生化试验和微阵列分析对肠道吸收和营养转运蛋白基因的表达的影响。将牛奶替代品的16个7天历史的健康仔猪随机分配给两组中的一个。 5天适应后,口服仔猪(n?=β8/组),用无菌盐水或PEDV(云南省的菌株)在10 4.5 tcid 50 每猪(50%组织培养剂量)。所有猪在PEDV或盐水给药后第5天口服D-木糖(0.1?G / kg BW)。一小时后,收集颈静脉血液样品以及肠样品进行进一步分析。与对照组相比,PEDV感染增加了腹泻发生率,血红素氧化酶活性和IFABP水平,同时降低仔猪中的生长和血浆D-木糖浓度。此外,PEDV感染改变了血浆和JEUNAL氨基酸谱,并降低了水蛋白和氨基酸转运蛋白的表达(L型氨基酸转运蛋白,钠型氨基酸转运蛋白,B(°,+ )-Type氨基酸输送蛋白,依赖依赖性中性氨基酸转运蛋白1,依赖依赖性谷氨酸/天冬氨酸转运蛋白3,以及肽转运蛋白(1),脂质转运和代谢相关基因(脂蛋白脂肪酶,脂蛋白A4,载脂蛋白A4,载脂蛋白C2,溶质载体家族27构件2,溶质载体家族27构件4,脂肪酸合酶和长链酰基-CoA合成酶(3),以及Jejunum中的葡萄糖输送基因(葡萄糖转运蛋白-2和胰岛素受体)。然而,PEDV给药增加磷酸丙酮酸羧基酶1,精氨酸琥珀酸合酶1,钠/葡萄糖共转运蛋白-1和囊性纤维化跨转运蛋白电导调节器的MRNA水平增加。集体,这些COMP缓解结果表明,PEDV感染诱导肠损伤,抑制编码营养转运蛋白的基因的表达。

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