TGEV infection up-regulates FcRn expression via activation of NF-κB signaling.
TGEV infection up-regulates FcRn expression via activation of NF-κB signaling.
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TGEV 感染通过激活 NF-κ B 信号传导上调 FcRn 表达
DOI：
10.1038/srep32154
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发表时间：
2016-08-24
影响因子：
4.6
通讯作者：
Li Z
中科院分区：
文献类型：
--
作者：
Guo J;Li F;Qian S;Bi D;He Q;Jin H;Luo R;Li S;Meng X;Li Z
新生儿Fc受体（FcRn）将母体IgG转运到胎儿或新生儿，并保护IgG不被降解。我们之前报道过FcRn在正常猪肠上皮细胞（IPEC-J2）模型中表达。传染性肠胃炎是由传染性肠胃炎病毒（TGEV）引起的猪急性肠道疾病。猪FcRn （pFcRn）的表达如何受到致病性感染的调控尚不清楚。我们的研究表明，感染TGEV的IPEC-J2细胞的pFcRn表达上调。此外，TGEV感染可激活IPEC-J2细胞的NF-κB信号通路。此外，用NF-κ b特异性抑制剂BAY 11-7082处理tgev感染的IPEC-J2细胞可下调pFcRn的表达。瞬时转染过表达NF-κB p65转录因子的pFcRn启动子荧光素酶报告质粒可增强荧光素酶报告质粒的激活。我们使用荧光素酶报告系统、染色质免疫沉淀、电迁移位移试验和超位移分析在该基因的启动子区域鉴定了4个NF-κB转录因子结合位点。总之，这些数据提供了TGEV感染通过激活NF-κB信号上调pFcRn表达的第一个证据。
It has been well characterized that the neonatal Fc receptor (FcRn) transports maternal IgG to a fetus or newborn and protects IgG from degradation. We previously reported that FcRn is expressed in a model of normal porcine intestinal epithelial cells (IPEC-J2). Transmissible gastroenteritis is an acute enteric disease of swine that is caused by transmissible gastroenteritis virus (TGEV). How porcine FcRn (pFcRn) expression is regulated by pathogenic infection remains unknown. Our research shows that IPEC-J2 cells infected with TGEV had up-regulated pFcRn expression. In addition, the NF-κB signaling pathway was activated in IPEC-J2 cells by TGEV infection. Furthermore, treatment of TGEV-infected IPEC-J2 cells with the NF-κB-specific inhibitor BAY 11-7082 resulted in down-regulation of pFcRn expression. Transient transfection of pFcRn promoter luciferase report plasmids with overexpression of NF-κB p65 transcription factor enhanced the activation of the luciferase report plasmids. We identified four NF-κB transcription factor binding sites in the promoter region of this gene using luciferase reporter system, chromatin immunoprecipitation, electromobility shift assay, and supershift analysis. Together, the data provide the first evidence that TGEV infection up-regulates pFcRn expression via activation of NF-κB signaling.