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肠炎沙门氏菌亚种肠炎沙门氏菌血清型肠炎沙门氏菌致病岛 2 型 III 型分泌系统:在鸡肠道定植和全身传播中的作用。

Salmonella enterica subspecies enterica serovar Enteritidis Salmonella pathogenicity island 2 type III secretion system: role in intestinal colonization of chickens and systemic spread.

机构信息

Vaccine and Infectious Disease Organization, University of Saskatchewan, 120 Veterinary Road, Saskatoon, SK, Canada S7N 5E3.

出版信息

Microbiology (Reading). 2010 Sep;156(Pt 9):2770-2781. doi: 10.1099/mic.0.038018-0. Epub 2010 May 20.

Abstract

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.

摘要

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。

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