Vaccine and Infectious Disease Organization, University of Saskatchewan, 120 Veterinary Road, Saskatoon, SK, Canada S7N 5E3.
Microbiology (Reading). 2010 Sep;156(Pt 9):2770-2781. doi: 10.1099/mic.0.038018-0. Epub 2010 May 20.
Salmonella enterica subspecies enterica serovar Enteritidis (S. Enteritidis) has been identified as a significant cause of salmonellosis in humans. Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2) each encode a specialized type III secretion system (T3SS) that enables Salmonella to manipulate host cells at various stages of the invasion/infection process. For the purposes of our studies we used a chicken isolate of S. Enteritidis (Sal18). In one study, we orally co-challenged 35-day-old specific pathogen-free (SPF) chickens with two bacterial strains per group. The control group received two versions of the wild-type strain Sal18: Sal18 attTn7 : : tet and Sal18 attTn7 : : cat, while the other two groups received the wild-type strain (Sal18 attTn7 : : tet) and one of two mutant strains. From this study, we concluded that S. Enteritidis strains deficient in the SPI-1 and SPI-2 systems were outcompeted by the wild-type strain. In a second study, groups of SPF chickens were challenged at 1 week of age with four different strains: the wild-type strain, and three other strains lacking either one or both of the SPI-1 and SPI-2 regions. On days 1 and 2 post-challenge, we observed a reduced systemic spread of the SPI-2 mutants, but by day 3, the systemic distribution levels of the mutants matched that of the wild-type strain. Based on these two studies, we conclude that the S. Enteritidis SPI-2 T3SS facilitates invasion and systemic spread in chickens, although alternative mechanisms for these processes appear to exist.
肠炎沙门氏菌亚种肠炎血清型(S. Enteritidis)已被确定为人类沙门氏菌病的重要病因。沙门氏菌致病岛 1 和 2(SPI-1 和 SPI-2)各自编码一种专门的 III 型分泌系统(T3SS),使沙门氏菌能够在入侵/感染过程的各个阶段操纵宿主细胞。在我们的研究中,我们使用了一株鸡源肠炎沙门氏菌(Sal18)。在一项研究中,我们将 35 日龄的无特定病原体(SPF)鸡同时用两种细菌株进行口服共挑战,每组 35 只。对照组接受两种野生型 Sal18 菌株:Sal18 attTn7::tet 和 Sal18 attTn7::cat,而另外两组则接受野生型菌株(Sal18 attTn7::tet)和两种突变株中的一种。从这项研究中,我们得出结论,SPI-1 和 SPI-2 系统缺陷的肠炎沙门氏菌菌株被野生型菌株所淘汰。在第二项研究中,SPF 鸡在 1 周龄时用四种不同的菌株进行挑战:野生型菌株,以及另外三种缺失 SPI-1 和 SPI-2 区的菌株。在攻毒后第 1 和第 2 天,我们观察到 SPI-2 突变株的全身传播减少,但到第 3 天,突变株的全身分布水平与野生型菌株相匹配。基于这两项研究,我们得出结论,肠炎沙门氏菌 SPI-2 T3SS 有助于在鸡中入侵和全身传播,尽管这些过程可能存在替代机制。