The transcription factor YbdO attenuates the pathogenicity of avian pathogenic Escherichia coli by regulating oxidative stress response.

IF 4 2区 生物学 Q2 MICROBIOLOGY
Lumin Yu, Yuzhong Zhao, Shanpeng Zhang, Linan Xu, Su Tang, Yuxuan Geng, Cong Xue, Xinglin Zhang
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引用次数: 0

Abstract

Avian pathogenic Escherichia coli (APEC) is a significant pathogen infecting poultry that is responsible for high mortality, morbidity and severe economic losses to the poultry industry globally, posing a substantial risk to the health of poultry. APEC encounters reactive oxygen species (ROS) during the infection process and thus has evolved antioxidant defense mechanisms to protect against oxidative damage. The imbalance of ROS production and antioxidant defenses is known as oxidative stress, which results in oxidative damage to proteins, lipids and DNA, and even bacterial cell death. APEC uses transcription factors (TFs) to handle oxidative stress. While many TFs in E. coli have been well characterized, the mechanism of the YbdO TF on protecting against oxidative damage and regulating the virulence and pathogenicity of APEC has not been clarified. Here we focus on the regulatory mechanism of YbdO on the pathogenicity of APEC. The results from this study showed that YbdO attenuated the pathogenicity of APEC in chicks infection models by inhibiting the expression of virulence genes fepG and ycgV using quantitative real-time reverse transcription PCR (RT-qPCR) experiments. The electrophoretic mobility shift assays (EMSA) confirmed that YbdO specifically bound to the promoters of fepG and ycgV. Additionally, YbdO increases H2O2-induced oxidative damage to APEC via repressing the expression of oxidative stress response genes sodA, soxR, ahpC, ahpF, katG, and oxyR by binding to their promoter regions. The repression effect facilitates host immune response to eliminate APEC and to generate beneficial immune protection to the body, thereby indirectly attenuating the pathogenicity of APEC. These findings might provide further insights into the mechanism of oxidative damage to APEC and offer new perspectives for further studies on the prevention and control of APEC infections.

转录因子YbdO通过调控氧化应激反应减弱禽致病性大肠杆菌的致病性。
禽致病性大肠杆菌(APEC)是一种感染家禽的重要病原体,对全球家禽业造成高死亡率、发病率和严重经济损失,对家禽健康构成重大风险。APEC在感染过程中会遇到活性氧(ROS),因此进化出抗氧化防御机制来保护机体免受氧化损伤。活性氧生成和抗氧化防御的失衡被称为氧化应激,它会导致蛋白质、脂质和DNA的氧化损伤,甚至细菌细胞死亡。APEC使用转录因子(TFs)来处理氧化应激。虽然大肠杆菌中的许多TF已经被很好地表征,但YbdO TF在抗氧化损伤和调节APEC毒力和致病性方面的机制尚不清楚。本文重点研究YbdO对APEC致病性的调控机制。本研究通过实时定量反转录PCR (RT-qPCR)实验发现,YbdO通过抑制毒力基因fepG和ycgV的表达,降低了APEC在鸡感染模型中的致病性。电泳迁移率转移实验(EMSA)证实YbdO特异性结合fepG和ycgV的启动子。此外,YbdO通过结合其启动子区域抑制氧化应激反应基因sodA、soxR、ahpC、ahpF、katG和oxyR的表达,从而增加h2o2诱导的对APEC的氧化损伤。这种抑制作用有利于宿主免疫应答消除APEC,对机体产生有益的免疫保护,从而间接减弱APEC的致病性。这些发现可能为进一步了解APEC氧化损伤的机制提供新的思路,并为进一步研究APEC感染的预防和控制提供新的视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
BMC Microbiology
BMC Microbiology 生物-微生物学
CiteScore
7.20
自引率
0.00%
发文量
280
审稿时长
3 months
期刊介绍: BMC Microbiology is an open access, peer-reviewed journal that considers articles on analytical and functional studies of prokaryotic and eukaryotic microorganisms, viruses and small parasites, as well as host and therapeutic responses to them and their interaction with the environment.
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