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作 者:段开放 邓雨明 崔桂梅[1] 彭其胜[1] DUAN Kai-fang,DENG Yu-ming,CUI Gui-mei,PENG Qi-sheng"(Key Laboratory for Zoonosis Research ,Ministry of Education, Institute of Zoonosis , Jilin University, Chang chun 130062, Chin)
机构地区:[1]吉林大学人兽共患病研究所教育部人兽共患病研究重点实验室
出 处:《中国兽医学报》2018年第3期528-531,共4页Chinese Journal of Veterinary Science
基 金:国家自然科学基金资助项目(31372409)
摘 要:布鲁菌病是一种典型的人兽共患细菌病,胞内寄生是其感染宿主、并难以治疗的主要原因。目前有关布鲁菌胞内寄生的机制尚未清晰。在本试验中,通过克隆布鲁菌DnaK基因到表达载体pQE-80L,分离纯化His-DnaK融合蛋白,探讨DnaK蛋白调节宿主细胞凋亡的功能。试验表明,第一,His-DnaK处理的巨噬细胞Caspase3剪切被抑制;第二,His-DnaK处理的巨噬细胞TUNEL染色显著降低;第三,布鲁菌DnaK蛋白能抑制宿主细胞凋亡。这将为进一步阐明布鲁菌胞内寄生的分子机制奠定基础。Brucellosis is one of the classical zoonotic diseases. Its virulence of Brucella depends on survival and replication properties in host cells. However, the underlying mechanism by which Brucella is able to grow within host cells remains unknown. Here,we investigate the role of DnaK of Brucella in mediating cell apoptosis via constructing the DnaK expression vector pQE-80L- DnaK and purifying the His-DnaK fusion proteins. Our data indicate that caspase3 cleavage is sup- pressed while macrophages are treated with His-DnaK. Consistent with Caspase-3 cleavage, our TUNEL experiments also show that the number of TUNEL staining of macrophages are significantly decreased compared with cisplatin treatment. These data suggest that DnaK of Brucella is able to inhibit cell apoptosis, which will lay solid background for further to study the molecular mechanism of intracellular survival of Brucella.
分 类 号:S852.65[农业科学—基础兽医学]
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