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TonB 和 Feo 介导的铁摄取对鼠伤寒沙门氏菌在小鼠体内生长的贡献。

Contribution of TonB- and Feo-mediated iron uptake to growth of Salmonella typhimurium in the mouse.

作者信息

Tsolis R M, Bäumler A J, Heffron F, Stojiljkovic I

机构信息

Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland 97201, USA.

出版信息

Infect Immun. 1996 Nov;64(11):4549-56. doi: 10.1128/iai.64.11.4549-4556.1996.

DOI:10.1128/iai.64.11.4549-4556.1996
PMID:8890205
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC174411/
Abstract

We examined the role of iron(II) and iron(III) uptake, mediated by FeoB and TonB, respectively, in infection of the mouse by Salmonella typhimurium. The S. typhimurium feoB gene, encoding a homolog of an Escherichia coli cytoplasmic membrane iron(II) permease, was cloned, and a mutant was generated by allelic exchange. In addition, an S. typhimurium tonB mutant was constructed. Together these two mutations inactivate all known iron uptake systems of S. typhimurium. We examined the abilities of these mutants to grow in vitro and in different compartments of the host. Mutants in feoB were outcompeted by the wild type during mixed colonization of the mouse intestine, but the feoB mutation did not attenuate S. typhimurium for oral or intraperitoneal infection of mice. The tonB mutation attenuated S. typhimurium for infection of mice by the intragastric route but not the intraperitoneal route, and the mutant was recovered in lower numbers from the Peyer's patches and mesenteric lymph nodes than the wild type. These results indicate that TonB-mediated iron uptake contributes to colonization of the Peyer's patches and mesenteric lymph nodes but not the liver and spleen of the mouse. The tonB feoB double mutant, given intraperitoneally, was able to infect the liver and spleen at wild-type doses, indicating that additional iron acquisition systems are used during growth at systemic sites of infection.

摘要

我们分别研究了由FeoB和TonB介导的亚铁离子(Fe²⁺)和铁离子(Fe³⁺)摄取在鼠伤寒沙门氏菌感染小鼠过程中的作用。编码大肠杆菌细胞质膜亚铁离子通透酶同源物的鼠伤寒沙门氏菌feoB基因被克隆,并通过等位基因交换产生了一个突变体。此外,构建了一个鼠伤寒沙门氏菌tonB突变体。这两个突变共同使鼠伤寒沙门氏菌所有已知的铁摄取系统失活。我们检测了这些突变体在体外和宿主不同区室中生长的能力。在小鼠肠道的混合定殖过程中,feoB突变体被野生型菌株竞争淘汰,但feoB突变并未使鼠伤寒沙门氏菌对小鼠的口服或腹腔感染减弱。tonB突变使鼠伤寒沙门氏菌通过胃内途径感染小鼠时减弱,但通过腹腔途径感染时未减弱,并且该突变体从派尔集合淋巴结和肠系膜淋巴结中回收的数量比野生型少。这些结果表明,TonB介导的铁摄取有助于在派尔集合淋巴结和肠系膜淋巴结中定殖,但对小鼠的肝脏和脾脏定殖没有作用。腹腔注射的tonB feoB双突变体能够以野生型剂量感染肝脏和脾脏,这表明在全身感染部位生长期间使用了额外的铁获取系统。

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