首页> 外文期刊>Infection and immunity >Role of SefA subunit protein of SEF14 fimbriae in the pathogenesis of Salmonella enterica serovar Enteritidis.
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Role of SefA subunit protein of SEF14 fimbriae in the pathogenesis of Salmonella enterica serovar Enteritidis.

机译:SEF14菌毛的SefA亚基蛋白在肠炎沙门氏菌肠炎沙门氏菌发病机理中的作用。

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In this study, the role of the SefA subunit protein of SEF14 fimbriae in the pathogenesis of Salmonella enterica serovar Enteritidis was investigated. This was accomplished by mutating the sefA gene in the chromosome of two strains of S. enterica serovar Enteritidis by allelic exchange with a copy that has been inactivated by interruption with a nonpolar kanamycin resistance (aphA-3) cassette. The effect of this mutation on the ability of the S. enterica serovar Enteritidis strains to colonize the intestinal epithelium and to invade other tissues was assessed in BALB/c mice and in vitro by adherence and invasion of HeLa cells. Our results show that an avirulent S. enterica serovar Enteritidis vaccine strain, 11RX (no somatic antigen; flagellum antigen phase 1, g,m; flagellum antigen phase 2, -), colonized better and persisted longer in the Peyer's patches of these mice than did its SefA-deficient counterpart. However, no such difference was observed between a highly virulent S. enterica serovar Enteritidis strain, 7314 (somatic antigen, O1, O9, O12; flagellum antigen phase 1, g,m; flagellum antigen phase 2 [1,7]), and its SefA-deficient isogenic mutant. These findings were correlated with in vitro adherence and invasion of HeLa cells. Furthermore, we could not demonstrate a role for SefA in the virulence of S. enterica serovar Enteritidis as assessed by 50% lethal dose determinations. The implications of these findings are discussed.
机译:在这项研究中,调查了SEF14菌毛的SefA亚基蛋白在肠炎沙门氏菌肠炎沙门氏菌发病机理中的作用。这是通过等位基因交换使两个肠炎链球菌血清肠炎沙门氏菌菌株的染色体中的sefA基因突变,并通过非极性卡那霉素抗性(aphA-3)盒中断而使该拷贝失活。在BALB / c小鼠中和在体外通过HeLa细胞的粘附和侵袭评估了该突变对肠炎链球菌肠炎沙门氏菌菌株定居肠道上皮和侵袭其他组织的能力的影响。我们的研究结果表明,无毒的肠炎链球菌血清肠炎沙门氏菌疫苗株11RX(无体抗原;鞭毛抗原1期,g,m;鞭毛抗原2期,-)在这些小鼠的Peyer斑块中的定植效果更好,并且持续时间更长做了SefA不足的对应程序。然而,在高毒力肠炎链球菌肠炎肠炎菌株7314(体抗原,O1,O9,O12;鞭毛抗原阶段1,g,m;鞭毛抗原阶段2 [1,7])和其SefA缺陷的同基因突变体。这些发现与HeLa细胞的体外粘附和侵袭有关。此外,通过50%致死剂量测定,我们无法证明SefA在肠炎链球菌肠炎沙门氏菌毒力中的作用。讨论了这些发现的含义。

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