Citrobacter rodentium virulence in mice associates with bacterial load and the type III effector NleE
Citrobacter rodentium virulence in mice associates with bacterial load and the type III effector NleE
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DOI：
10.1016/j.micinf.2006.12.016
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发表时间：
2007-03-01
影响因子：
5.8
通讯作者：
Finlay, B. Brett
中科院分区：
文献类型：
--
作者：
Wickham, Mark E.;Lupp, Claudia;Finlay, B. Brett
由产滋贺毒素大肠杆菌（STEC）引起的严重疾病与致病性岛O岛122相关，O岛122编码III型分泌系统效应物NleE。在这里，我们表明，相关的附着和消失的小鼠病原体啮齿类柠檬酸杆菌的全部毒力需要NleE。相对于野生型细菌，nleE突变体C.啮齿类动物在单一和混合感染中在小鼠中的定殖均减毒。对nleE突变体细菌在体内诱导病理变化的能力的检查显示，在易感小鼠中，nleE突变体细菌诱导的病理变化显著低于野生型细菌。与这些结果一致，感染nleE突变细菌的小鼠表现出延迟死亡。结果提示，病原体感染和消退过程中的病理变化可能与病原体定植的程度有关。使用23个III型分泌基因的突变体，包括III型效应子nleC、nleD、nleE和nleF，检查病理变化与这些突变体定殖小鼠的能力的关联。体内疾病的诱导与定殖程度密切相关，表明定殖优势III型分泌基因提供细菌，有助于完全毒力，并且是完全毒力所需的。(c)2007年由Elsevier Masson SAS出版。
Severe disease caused by Shiga toxin-producing Escherichia coli (STEC) has been associated with a pathogenicity island, O-Island 122, which encodes the type III secretion system-effector NleE. Here we show that full virulence of the related attaching and effacing mouse pathogen Citrobacter rodentium requires NleE. Relative to wild-type bacteria, nleE-mutant C. rodentium are attenuated for colonisation in mice in both single and mixed infections. Examination of the ability of nleE-mutant bacteria to induce pathologic change in vivo revealed that nleE-mutant bacteria induce significantly less pathologic change than wild-type bacteria in susceptible mice. Consistent with these results, mice infected with nleE-mutant bacteria exhibit delayed mortality. These results suggested that pathologic change during attaching and effacing pathogen infection may associate with the degree of pathogen colonisation. Using mutants of 23 type III secretion genes, including the type III effectors nleC, nleD, nleE and nleF, the association of pathologic change with the ability of these mutants to colonise mice was examined. The induction of in vivo disease correlates strongly with the degree of colonisation, suggesting that the colonisation advantage type III secretion genes afford the bacteria, contribute to, and are required for, full virulence. (c) 2007 Published by Elsevier Masson SAS.