作 者：
石勇丽;谢芝勋;罗思思;韦悠;王盛;任红玉;谢丽基;万丽军;李孟;黄娇玲
单 位：
广西大学动物科学技术学院;广西壮族自治区兽医研究所广西兽医生物技术重点实验室
关键词：
血清4型禽腺病毒(FAdV-4);LMH细胞;Toll样受体;实时荧光定量PCR
摘 要：
为了解血清4型禽腺病毒(FAdV-4)感染宿主后对Toll样受体(TLRs)转录水平的影响,本研究用FAdV-4感染鸡肝癌细胞(LMH),收集感染后第12、24、36、48、60、72、84、96、108、120小时的细胞样品,利用荧光定量PCR技术监测FAdV-4的复制情况和10种TLRs(TLR1a、TLR1b、TLR2a、TLR2b、TLR3、TLR4、TLR5、TLR7、TLR15、TLR21)的m RNA转录水平动态变化。结果显示,FAdV-4感染LMH细胞后,细胞出现变亮、变圆和脱落等典型病变,病毒在12～48 h快速增殖,随后缓慢增殖至120 h,10种TLRs均出现不同程度上调,感染后期(72～120 h)上调尤为剧烈(P<0.05或P<0.01),其中TLR1a、TLR1b、TLR4、TLR7和TLR21上调幅度较大,分别上调26.06倍、24.37倍、38.56倍、17.97倍、56.71倍。表明TLRs在宿主抵抗FAdV-4感染过程中起关键作用,该结果为今后深入探究FAdV-4的致病机理提供了参考依据。
译 名：
Dynamic changes of mRNA transcription levels of Toll-like receptors of fowl adenovirus serotype 4 infected LMH cells
作 者：
SHI Yong-li;XIE Zhi-xun;LUO Si-si;WEI You;WANG Sheng;REN Hong-yu;XIE Li-ji;WAN Li-jun;LI Meng;HUANG Jiao-ling;College of Animal Science and Technology,Guangxi University;Guangxi Key Laboratory of Veterinary Biotechnology,Guangxi Veterinary Research Institute;
关键词：
fowl adenovirus serotype 4;;LMH cells;;toll-like receptors;;real-time PCR
摘 要：
In order to understand the effect of fowl adenovirus serotype 4 infection on toll-like receptor(TLRs) transcription level,FAd V-4 was used to infect LMH cells,and cell samples were collected12,24,36,48,60,72,84,96,108,120 h after infection.The m RNA transcription levels of 10 TLRs(TLR1 a,TLR1 b,TLR2 a,TLR2 b,TLR3,TLR4,TLR5,TLR7,TLR15,TLR21) were detected by real-time PCR.The results showed that FAd V-4 infected LMH cells showed typical pathological changes,such as brightening,roundness and shedding.The virus rapidly proliferated in 12—48 h,and then slowly proliferated to 120 h.The 10 TLRs were all upregulated to varying degrees,especially in the later infection period(72—120 h,P<0.05 or P<0.01).Among them,TLR1 a,TLR1 b,TLR4,TLR7 and TLR21 upregulated significantly by 26.06,24.37,38.56,17.97,56.71 times,respectively.These results indicate that TLRs plays a vital role in the host resistance to FAd V-4 infection,which provides a reference for further exploration of the pathogenesis of FAd V-4.
