猪链球菌丝氨酸/苏氨酸激酶基因缺失株的构建及其致病性

Construction of serine/threonine kinase gene knock-out mutant of Streptococcus suis and its pathogenicity

为了研究丝氨酸/苏氨酸磷激酶(STK)在猪链球菌致病过程中的作用,利用大肠杆菌-猪链球菌穿梭质粒p SET4s构建STK基因缺失株△stk。结果显示,stk基因缺失后,缺失株△stk易形成长链状结构;缺失株的半致死剂量(LD50)较亲本株高7倍,对CD1小鼠的致病能力降低;体内定植试验结果表明缺失株△stk在小鼠体内各器官的定植能力显著降低。这些数据表明STK与猪链球菌2型(SS2)的致病性相关。

To investigate the role of the analogous serine/threonine kinases（STK） in Streptococcus suis infection,an isogenic STK mutant（△stk） was constructed by using Escherichia.coli-S.suis shuttle vector p SET4 s.The mutant strain exhibited a long chain formation.The △stk was attenuated in a CD1 murine model of infection and its LD50 values was seventimes higher than that of the wild type.In vivo colonization experiments showed the significantly reduced bacterial colonization of △stk in tissues.It is indicated that the STK is involved in the pathogenicity of Streptococcus suis type 2（SS2）.