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产肠毒素大肠杆菌K88诱导仔猪炎症反应的分子机制
引用本文:李海花,朱琪,王世琼,杨春蕾,赵向华,乔家运,王文杰.产肠毒素大肠杆菌K88诱导仔猪炎症反应的分子机制[J].中国畜牧兽医,2017,44(1):262-267.
作者姓名:李海花  朱琪  王世琼  杨春蕾  赵向华  乔家运  王文杰
作者单位:1. 天津市畜牧兽医研究所, 天津 300381;
2. 天津市畜禽健康养殖技术工程中心, 天津 300381
基金项目:国家自然科学基金(31402087)
摘    要:为探讨产肠毒素大肠杆菌(ETEC) K88感染仔猪发生炎症反应的分子机制,试验用ETEC K88灌服断奶仔猪,ELISA法检测攻毒后仔猪血清中白细胞介素8(IL-8)含量,实时荧光定量PCR方法检测淋巴结中Toll样受体2(TLR2)、Toll样受体4(TLR4)及其信号通路相关基因(髓样分化因子88(MyD88)、Toll相互作用蛋白(Tollip)、B细胞淋巴瘤因子3(Bcl3))的mRNA相对表达水平。结果发现,仔猪攻毒ETEC K88后6和24 h血清IL-8含量和淋巴结TLR2/4的表达水平均极显著或显著高于对照组(P<0.01;P<0.05),且感染后24 h显著低于感染后6 h(P<0.05);仔猪感染ETEC K88后24 h淋巴结中MyD88、Tollip和Bcl3的表达水平均极显著高于对照组(P<0.01),但是感染后6 h时与对照组相比均无显著差异(P>0.05)。综上所述,ETEC K88感染仔猪可能是通过TLR2/4-MyD88信号通路产生炎症因子IL-8,促使仔猪出现炎症反应,且该炎症反应可能受Tollip和Bcl3蛋白的调控而被减弱。

关 键 词:大肠杆菌K88  仔猪  炎症反应  Toll-样受体  炎症调控  
收稿时间:2016-06-14

Molecular Mechanism of the Inflammatory Response Induced by Enterotrxigenic E. coli K88 in Piglets
LI Hai-hua,ZHU Qi,WANG Shi-qiong,YANG Chun-lei,ZHAO Xiang-hua,QIAO Jia-yun,WANG Wen-jie.Molecular Mechanism of the Inflammatory Response Induced by Enterotrxigenic E. coli K88 in Piglets[J].China Animal Husbandry & Veterinary Medicine,2017,44(1):262-267.
Authors:LI Hai-hua  ZHU Qi  WANG Shi-qiong  YANG Chun-lei  ZHAO Xiang-hua  QIAO Jia-yun  WANG Wen-jie
Institution:1. Tianjin Institute of Animal Husbandry and Veterinary Science, Tianjin 300381, China;
2. Tianjin Engineering Research Center for Livestock and Poultry Health Breeding, Tianjin 300381, China
Abstract:To investigate the molecular mechanism of the inflammatory response in the piglets infected with enterotoxigenic E. coli (ETEC) K88, piglets were infected with ETEC K88,the IL-8 content in serum of piglets were assayed by ELISA,and the mRNA relative expression levels of TLR2/4 and its signal transduction pathway related genes (MyD88,Tollip and Bcl3) in mesenteric lymph nodes were detected by quantitative Real-time PCR. The results showed that compared with control group,the content of IL-8 in serum and the expressions of TLR2/4 in lymph nodes were all extremely significantly or significantly increased at 6 and 24 h after infection (P<0.01;P<0.05),and the IL-8 content and TLR2/4 mRNA expression at 24 h after infection were all significantly lower than those at 6 h after infection (P<0.05).In addition,the expressions of MyD88,Tollip and Bcl3 in lymph nodes were all extremely significantly increased at 24 h after infection compared with control group (P<0.01), but there was no significant difference between experimental group and control group at 6 h after infection (P>0.05). In conclusion,ETEC K88 infected piglets might produce inflammatory cytokines IL-8 through the TLR2/4-MyD88 signaling pathway,which could promote the inflammatory reaction in piglets. This inflammatory response might be regulated by Tollip and Bcl3,which could weak the inflammatory intensity in piglets.
Keywords:E  coli K88  piglet  inflammatory response  Toll-like receptors  inflammatory regulation  
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