SodA Contributes to the Virulence of Avian Pathogenic Escherichia coli O2 Strain E058 in Experimentally Infected Chickens
SodA Contributes to the Virulence of Avian Pathogenic Escherichia coli O2 Strain E058 in Experimentally Infected Chickens
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SodA 有助于增强实验感染鸡中禽致病性大肠杆菌 O2 菌株 E058 的毒力
DOI：
10.1128/jb.00625-18
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发表时间：
2019-03-01
影响因子：
3.2
通讯作者：
Gao, Song
中科院分区：
文献类型：
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作者：
Gao, Qingqing;Xia, Le;Gao, Song
禽大肠杆菌病是由禽源性大肠杆菌引起的一种重要的细菌性疾病，对世界范围内的养禽业具有严重的经济意义。APEC的毒力机制尚未完全了解。本研究探讨了抗氧化蛋白SodA对APEC O2菌株E058的表型和致病性的影响。这是第一份报告表明，SodA起着重要的作用，在保护一个特定的APEC菌株对过氧化氢诱导的氧化应激，并有助于这种致病型菌株的毒力。这种毒力因子的鉴定将提高我们对APEC致病机制的认识，这对于设计成功的抗相关感染和传播策略至关重要。摘要禽致病性大肠杆菌（APEC）是禽大肠杆菌病的常见病原菌，在感染过程中会产生活性氧。超氧化物歧化酶（SOD）作为抗氧化因子，可以对抗ROS介导的宿主防御。我们以前的报告表明，sodA基因（编码锰辅因子，含SOD [MnSOD]）是高表达的败血症感染过程中的APEC。sodA已被证明是某些病原体的毒力因子，但其在APEC致病性中的作用尚未完全确定。在这项研究中，我们删除了sodA基因的毒力APEC O2株E058，并在体外和体内的突变表型进行了研究。的sodA突变体是更敏感的过氧化氢在其增长和活力比野生型。在sodA突变体中形成生物膜的能力减弱。sodA突变体比野生型菌株更容易被鸡巨噬细胞吞噬。鸡感染试验表明，显着减弱的毒力的sodA突变体相比，野生型在感染后24小时。毒力表型通过sodA基因的互补而恢复。实时定量逆转录PCR结果显示，sodA的失活降低了氧化应激反应基因katE、perR和osmC的表达，但不影响sodB和sodC的表达。总之，我们的研究表明，SodA是重要的抗氧化性和毒性的APEC E058。重要性禽大肠杆菌病是由禽致病性大肠杆菌菌株引起的一种主要细菌性疾病，对全球家禽业具有严重的经济意义。APEC的毒力机制尚未完全了解。本研究探讨了抗氧化蛋白SodA对APEC O2菌株E058的表型和致病性的影响。这是第一份报告表明，SodA起着重要的作用，在保护一个特定的APEC菌株对过氧化氢诱导的氧化应激，并有助于这种致病型菌株的毒力。这种毒力因子的鉴定将提高我们对APEC致病机制的认识，这对于设计成功的抗相关感染和传播策略至关重要。
Avian colibacillosis, caused by strains of avian pathogenic Escherichia coli, is a major bacterial disease of severe economic significance to the poultry industry worldwide. The virulence mechanisms of APEC are not completely understood. This study investigated the influence of an antioxidant protein, SodA, on the phenotype and pathogenicity of APEC O2 strain E058. This is the first report demonstrating that SodA plays an important role in protecting a specific APEC strain against hydrogen peroxide-induced oxidative stress and contributes to the virulence of this pathotype strain. Identification of this virulence factor will enhance our knowledge of APEC pathogenic mechanisms, which is crucial for designing successful strategies against associated infections and transmission. ABSTRACT Strains of avian pathogenic Escherichia coli (APEC), the common pathogen of avian colibacillosis, encounter reactive oxygen species (ROS) during the infection process. Superoxide dismutases (SODs), acting as antioxidant factors, can protect against ROS-mediated host defenses. Our previous reports showed that the sodA gene (encoding a Mn-cofactor-containing SOD [MnSOD]) is highly expressed during the septicemic infection process of APEC. sodA has been proven to be a virulence factor of certain pathogens, but its role in the pathogenicity of APEC has not been fully identified. In this study, we deleted the sodA gene from the virulent APEC O2 strain E058 and examined the in vitro and in vivo phenotypes of the mutant. The sodA mutant was more sensitive to hydrogen peroxide in terms of both its growth and viability than was the wild type. The ability to form a biofilm was weakened in the sodA mutant. The sodA mutant was significantly more easily phagocytosed by chicken macrophages than was the wild-type strain. Chicken infection assays revealed significantly attenuated virulence of the sodA mutant compared with the wild type at 24 h postinfection. The virulence phenotype was restored by complementation of the sodA gene. Quantitative real-time reverse transcription-PCR revealed that the inactivation of sodA reduced the expression of oxidative stress response genes katE, perR, and osmC but did not affect the expression of sodB and sodC. Taken together, our studies indicate that SodA is important for oxidative resistance and virulence of APEC E058. IMPORTANCE Avian colibacillosis, caused by strains of avian pathogenic Escherichia coli, is a major bacterial disease of severe economic significance to the poultry industry worldwide. The virulence mechanisms of APEC are not completely understood. This study investigated the influence of an antioxidant protein, SodA, on the phenotype and pathogenicity of APEC O2 strain E058. This is the first report demonstrating that SodA plays an important role in protecting a specific APEC strain against hydrogen peroxide-induced oxidative stress and contributes to the virulence of this pathotype strain. Identification of this virulence factor will enhance our knowledge of APEC pathogenic mechanisms, which is crucial for designing successful strategies against associated infections and transmission.