【摘 要】
：
鼠伤寒沙门菌表达两个不同的Ⅲ型分泌系统(typeⅢsecretion/translocation systems,TTSS),分别由致病岛1和2(pathogenicity islands 1 and 2,SPI-1 and SPI-2)编码.细菌依赖T
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鼠伤寒沙门菌表达两个不同的Ⅲ型分泌系统(typeⅢsecretion/translocation systems,TTSS),分别由致病岛1和2(pathogenicity islands 1 and 2,SPI-1 and SPI-2)编码.细菌依赖TTSS将效应蛋白转运至宿主细胞,通过"触发"机制诱导细菌进入宿主细胞.这些效应蛋白可诱导细胞骨架重排,导致"巨吞饮",促使细菌入侵.本综述依据多种沙门菌效应蛋白的功能,建立沙门菌侵袭模型.TTSS活化并转运效应蛋白进入宿主细胞发挥功能(Ⅰ).小G蛋白交换因子SopE和肌醇磷酸酯酶SopB通过激活CDC42和Racl,诱导内陷相关的蛋白聚集(Ⅱ).SipA和SipC通过降低肌动蛋白临界浓度、刺激网素成柬、稳定纤维状肌动蛋白(fibrousactin,F-actin)以及使肌动蛋白核化等功能,促使细菌入侵(Ⅲ).SopB可使膜内陷区PIP2的浓度降低以及VAMP8聚集,促使细胞膜分裂(Ⅳ).这些效应蛋白的联合作用,使膜皱褶在局部向外显著延伸,使沙门菌被细胞内形成的特殊膜结构包裹.沙门菌的另一种效应蛋白SptP,通过刺激小G蛋白内源性GTPase的活性,抑制小G蛋白的活化,使细胞膜恢复至原有状态(Ⅴ).
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