Role of outer membrane protein T in pathogenicity of avian pathogenic Escherichia coli
Role of outer membrane protein T in pathogenicity of avian pathogenic Escherichia coli
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外膜蛋白T在禽致病性大肠杆菌致病性中的作用
DOI：
10.1016/j.rvsc.2017.01.026
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发表时间：
2017-12-01
影响因子：
2.4
通讯作者：
Yao, Huochun
中科院分区：
文献类型：
--
作者：
Hejair, Hassan M. A.;Ma, Jiale;Yao, Huochun
外膜蛋白T （OmpT）可能在人和动物新生儿脑膜炎大肠杆菌（NMEC）的发病机制中起重要作用。然而，ompT是否在禽致病性E. coil （APEC）感染中起作用尚不清楚。在这项研究中，我们评估了ompT在APEC发病机制中的潜力。从APEC突变株TW-XM中缺失了一个ompTgene，并对其进行了结构分析。ompT的失活显著降低了APEC对小鼠脑微血管内皮细胞（BMEC） bEnd的粘附和侵袭能力。与野生菌株TW-XM相比，细胞增殖率分别为43.8%和28.8%。进一步的研究表明，基于LD50的测量，ompT基因的缺失在雏鸭中降低了15.2倍的细菌毒力，在小鼠模型中降低了9.7倍。此外，对动物的实验感染表明，与野生型菌株TW-XM相比，ompT的缺失使APEC在脑、肺和血液中的定植和入侵能力分别降低了2倍、1.96倍和1.7倍。这些毒力相关表型部分可通过遗传互补恢复。定量实时逆转录pcr （qRT-PCR）结果显示，与TW-XM相比，缺失ompT显著降低了突变株Delta ompT中ompA、fimC和tsh的表达量（p < 0.01）。总的来说，我们的数据表明，ompT的失活可能通过降低ompA、fimC和tsh的表达水平来降低粘附、侵袭、定植和增殖能力，这可能证明ompT与APEC致病性有关。(C) 2017 Elsevier Ltd.版权所有。
An outer membrane protein T (OmpT) could play a vital role in the pathogenesis of the neonatal meningitis Escherichia coli (NMEC) in human and animals. However, whether ompT plays a role in avian pathogenic E. coil (APEC) infection remains unclear. In this study we evaluated the potential of ompT in APEC pathogenesis. An ompTgene was deleted from APEC mutant strain (TW-XM) was constructed and characterized. The inactivation of ompT reduced significantly the adherence and invasion capabilities of APEC to mouse brain microvascular endothelial cell (BMEC) bEnd.3 cells at the rates of 43.8% and 28.8% respectively, compared with the wild strain TW-XM. Further studies showed that deletion of ompT gene reduced the bacterial virulence with 15.2-fold in ducklings and 9.7-fold in mouse models based on the measurement of the LD50. Furthermore, experimental infection of animals revealed that, loss of ompT showed reduced APEC colonization and invasion capacity in brains, lungs and blood by 2-fold, 1.96-fold, and 1.7-fold, respectively, compared with the wild-type strain TW-XM. These virulence-related phenotypes were partially recoverable by genetic complementation. The results of the quantitative real-time reverse transcription-PCR (qRT-PCR) indicated that the loss of ompT significantly decreased the expression levels of ompA, fimC and tsh in the mutant strain Delta OmpT, when compared with TW-XM (p < 0.01). Collectively, our data showed that inactivation of ompT decreased adhesion, invasion, colonization, proliferation capacities, possibly by reduced expression levels of ompA, fimC and tsh, which may justify that, ompT is implicated in APEC pathogenicity. (C) 2017 Elsevier Ltd. All rights reserved.