PRRSV在感染早期通过活化CREB竞争抑制p65与CBP结合
文献类型: 中文期刊
作者: 李先斌;王鑫;谭祥梅;陈鹏飞;赵雄伟;吴瑕;虞凌雪;高飞;姜一峰;于海;童光志;周艳君
作者机构:
关键词: 高致病性猪繁殖与呼吸综合征病毒;CREB;p65;CBP;IFN-β
期刊名称:中国预防兽医学报
ISSN: 1008-0589
年卷期: 2019 年 7 期
页码: 670-676
收录情况: 北大核心(2020版) ; CSCD(2020-2021年度) ; 农林核心(2020版) ; 科技核心(2020版)
摘要: 为研究细胞内cAMP反应元件结合蛋白(CREB)的结合蛋白(CBP)在高致病性猪繁殖与呼吸综合征病毒(HP-PRRSV)感染后的结合动态对I型干扰素(IFN-I)表达的影响,本研究利用HP-PRRSV强毒Hu N4株感染宿主细胞,采用CO-IP方法分析CREB的磷酸化情况及其结合动态.结果显示Hu N4株感染猪肺泡巨噬细胞(PAMs)能够引起CREB明显磷酸化,Hu N4株感染PAMs和Marc-145细胞使p38磷酸化水平显著上调,PKA通路抑制剂可以明显抑制Marc-145细胞中CREB的磷酸化水平,但不影响PAMs中CREB的磷酸化水平.并且Hu N4株感染Marc-145细胞1 h后磷酸化的CREB能够与CBP结合,并抑制了p65与CBP的结合.当抑制剂H-89和SB203580抑制Marc-145细胞中CREB的磷酸化后,CREB与CBP的结合同时受到抑制.本研究表明HP-PRRSV Hu N4株感染细胞后,可以通过激活p38 MAPK通路而活化CREB,活化的CREB与p65竞争结合CBP,而抑制p65与CBP的结合,使得HP-PRRSV在感染早期抑制了IFN-β的表达.本研究为深入研究HP-PRRSV的免疫抑制机理提供了实验依据.
分类号: S858.28
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