Escherichia coli type III secretion system 2 regulator EtrA promotes virulence of avian pathogenic Escherichia coli

文献类型： 外文期刊

第一作者： Wang, Shaohui

作者： Wang, Shaohui;Xu, Xuan;Liu, Xin;Wang, Dong;Liang, Hua;Wu, Xiaojun;Tian, Mingxing;Ding, Chan;Yu, Shengqing;Xu, Xuan;Wang, Guijun

作者机构：

关键词： avian pathogenic Escherichia coli;EtrA;regulator;intracellular survival;virulence

期刊名称：MICROBIOLOGY-SGM （ 影响因子：2.777； 五年影响因子：2.871 ）

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收录情况： SCI

摘要： The Escherichia coli type III secretion system 2 (ETT2) is found in most E. coli strains, including pathogenic and commensal strains. Although many ETT2 gene clusters carry multiple genetic mutations or deletions, ETT2 is known to be involved in bacterial virulence. In enterohaemorrhagic E. coli (EHEC), ETT2 affects adhesion through the regulator EtrA, which regulates transcription and secretion of the type III secretion system (T3SS) encoded by the locus of enterocyte effacement (LEE). To date, no studies have been conducted on the role of EtrA in the virulence of avian pathogenic E. coli (APEC), which harbours only ETT2. Thus, we constructed etrA mutant and complemented strains of APEC and evaluated their phenotypes and pathogenicities. We found that the etrA gene deletion significantly reduced bacterial survival in macrophages, and proliferation and virulence in ducks. In addition, the etrA gene deletion reduced expression of the APEC fimbriae genes. Upregulation of genes encoding the pro-inflammatory cytokines interleukin (IL)-1 beta and IL-8 was also observed in HD-11 macrophages infected with the etrA gene mutant strain compared to the wild-type strain. Furthermore, the altered capacities of the mutant strain were restored by genetic complementation. Our observations demonstrate that the ETT2 regulator EtrA contributes to the virulence of APEC.

分类号： Q93

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