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【目的】探索沙门菌在进化过程中通过水平转移获得的未知功能岛在其致病过程中的作用,发现新的与致病性相关的岛。【方法】以鼠伤寒沙门菌ATCC 14028为亲本株,利用λRed重组酶系统分别构建了7个未知功能岛(STM14_0667-0673、2682-2687、2885-2891、3721-3728、4247-4253、4823-4828、5331-5341)的突变株,通过细胞侵袭实验、巨噬细胞内复制力检测及小鼠实验比较了野生型和突变株的毒力差异。【结果】Δ2682-2687和Δ5331-5341对上皮细胞的侵袭力显著低于野生型(P<0.01);Δ2682-2687、Δ2885-2891和Δ5331-5341在巨噬细胞内的复制力、对小鼠的致死率以及在小鼠肠道和肝、脾的定殖能力均显著低于野生型(P<0.05);其余4个突变株(Δ0667-0673、Δ3721-3728、Δ4247-4253、Δ4823-4828)的侵袭力、胞内复制力以及对小鼠的致病力与野生型相比无显著差异。【结论】发现3个未知功能岛显著影响鼠伤寒沙门菌的致病力,为深入研究这些岛的功能及调控机制奠定了基础。
【Objective】 The purpose of this study was to explore the role of unknown functional island derived from Salmonella in the process of evolution by horizontal transfer during its pathogenicity and to discover new pathogenic related islands. 【Method】 Using Salmonella typhimurium ATCC 14028 as the parent strain, seven unknown functional islands (STM14_0667-0673, 2682-2687, 2885-2891, 3721-3728, 424-7-4253, 4823- 4828,5331-5341). The differences of virulence between wild-type and mutant strains were compared by cell invasion assay, macrophage replication assay and mouse experiment. 【Results】 The invasiveness of epithelial cells of Δ2682-2687 and Δ5331-5341 was significantly lower than that of wild type (P <0.01). The replicative power of Δ2682-2687, Δ2885-2891 and Δ5331-5341 in macrophages were significantly decreased (P <0.05). The other four mutants (Δ0667-0673, Δ3721-3728, Δ4247-4253, Δ4823-4828 ) Invasiveness, intracellular replication and virulence in mice compared with the wild-type no significant difference. 【Conclusion】 Three unknown functional islands were found to significantly affect the virulence of S. typhimurium, which lays the foundation for further study on the functions and regulatory mechanisms of these islands.