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Abstract：
BACKGROUND: The pathogenicity of Helicobacter pylori is dependent on factors including the environment and the host. Although selenium is closely related to pathogenicity as an environmental factor, the specific correlation between them remains unclear.
OBJECTIVE: To investigate how selenium acts on virulence factors and reduces their toxicity.
METHODS: H. pylori strains were induced by sodium selenite. The expression of cytotoxin-associated protein A (CagA) and vacuolating cytotoxin gene A (VacA) was determined by quantitative PCR and Western blotting. Transcriptomics was used to analyze CagA, CagM, CagE, Cag1, Cag3, and CagT. C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction, and H. pylori colonization, inflammatory reactions, and the cell adhesion ability of H. pylori were assessed.
RESULTS: CagA and VacA expression was upregulated at first and then downregulated in the H. pylori strains after sodium selenite treatment. Their expression was significantly and steadily downregulated after the 5th cycle (10 d). Transcriptome analysis revealed that sodium selenite altered the levels affect H. pylori virulence factors such as CagA, CagM, CagE, Cag1, Cag3, and CagT. Of these factors, CagM and CagE expression was continuously downregulated and further downregulated after 2 h of induction with sodium selenite. Moreover, CagT expression was upregulated before the 3rd cycle (6 d) and significantly downregulated after the 5th cycle. Cag1 and Cag3 expression was upregulated and downregulated, respectively, but no significant change was observed by the 5th cycle. C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction. The extent of H. pylori colonization in the stomach increased; however, sodium selenite also induced a mild inflammatory reaction in the gastric mucosa of H. pylori-infected mice, and the cell adhesion ability of H. pylori was significantly weakened.
CONCLUSIONS: These results demonstrate that H. pylori displayed virulence attenuation after the 10th d of sodium selenite treatment. Sodium selenite is a low toxicity compound with strong stability that can reduce the cell adhesion ability of H. pylori, thus mitigating the inflammatory damage to the gastric mucosa.
OBJECTIVE: To investigate how selenium acts on virulence factors and reduces their toxicity.
METHODS: H. pylori strains were induced by sodium selenite. The expression of cytotoxin-associated protein A (CagA) and vacuolating cytotoxin gene A (VacA) was determined by quantitative PCR and Western blotting. Transcriptomics was used to analyze CagA, CagM, CagE, Cag1, Cag3, and CagT. C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction, and H. pylori colonization, inflammatory reactions, and the cell adhesion ability of H. pylori were assessed.
RESULTS: CagA and VacA expression was upregulated at first and then downregulated in the H. pylori strains after sodium selenite treatment. Their expression was significantly and steadily downregulated after the 5th cycle (10 d). Transcriptome analysis revealed that sodium selenite altered the levels affect H. pylori virulence factors such as CagA, CagM, CagE, Cag1, Cag3, and CagT. Of these factors, CagM and CagE expression was continuously downregulated and further downregulated after 2 h of induction with sodium selenite. Moreover, CagT expression was upregulated before the 3rd cycle (6 d) and significantly downregulated after the 5th cycle. Cag1 and Cag3 expression was upregulated and downregulated, respectively, but no significant change was observed by the 5th cycle. C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction. The extent of H. pylori colonization in the stomach increased; however, sodium selenite also induced a mild inflammatory reaction in the gastric mucosa of H. pylori-infected mice, and the cell adhesion ability of H. pylori was significantly weakened.
CONCLUSIONS: These results demonstrate that H. pylori displayed virulence attenuation after the 10th d of sodium selenite treatment. Sodium selenite is a low toxicity compound with strong stability that can reduce the cell adhesion ability of H. pylori, thus mitigating the inflammatory damage to the gastric mucosa.
摘要：
背景：幽门螺杆菌的致病性取决于环境和宿主等因素。尽管硒作为环境因素与致病性密切相关，它们之间的具体相关性尚不清楚.
目的：研究硒如何作用于毒力因子并降低其毒性。
方法：H.亚硒酸钠诱导幽门螺杆菌菌株。通过定量PCR和Western印迹测定细胞毒素相关蛋白A（CagA）和空泡细胞毒素基因A（VacA）的表达。转录组学用于分析CagA，CagM,卡格,Cag1、Cag3和CagT。用亚硒酸钠诱导的减毒株感染C57BL/6A小鼠，和幽门螺杆菌定植，炎症反应，并对幽门螺杆菌的细胞粘附能力进行了评估。
结果：在亚硒酸钠处理后，幽门螺杆菌菌株中CagA和VacA的表达首先上调，然后下调。在第5个周期（10d）后，它们的表达显着稳定地下调。转录组分析显示，亚硒酸钠改变了影响幽门螺杆菌毒力因子如CagA的水平，CagM,卡格,Cag1、Cag3和CagT。在这些因素中,CagM和CagE表达连续下调，用亚硒酸钠诱导2小时后进一步下调。此外，CagT表达在第3个周期（6d）前上调，第5个周期后显著下调。Cag1和Cag3表达上调和下调，分别,但是在第5个周期没有观察到明显的变化。用经过亚硒酸钠诱导的减毒株感染C57BL/6A小鼠。幽门螺杆菌在胃中定植的程度增加；然而，亚硒酸钠还在幽门螺杆菌感染小鼠的胃粘膜中诱导轻度炎症反应，H.pylori的细胞粘附能力明显减弱。
结论:这些结果表明幽门螺杆菌在第10天的亚硒酸钠处理后显示出毒力减弱。亚硒酸钠是一种低毒性化合物，具有很强的稳定性，可以降低幽门螺杆菌的细胞粘附能力，从而减轻对胃粘膜的炎症损伤。
目的：研究硒如何作用于毒力因子并降低其毒性。
方法：H.亚硒酸钠诱导幽门螺杆菌菌株。通过定量PCR和Western印迹测定细胞毒素相关蛋白A（CagA）和空泡细胞毒素基因A（VacA）的表达。转录组学用于分析CagA，CagM,卡格,Cag1、Cag3和CagT。用亚硒酸钠诱导的减毒株感染C57BL/6A小鼠，和幽门螺杆菌定植，炎症反应，并对幽门螺杆菌的细胞粘附能力进行了评估。
结果：在亚硒酸钠处理后，幽门螺杆菌菌株中CagA和VacA的表达首先上调，然后下调。在第5个周期（10d）后，它们的表达显着稳定地下调。转录组分析显示，亚硒酸钠改变了影响幽门螺杆菌毒力因子如CagA的水平，CagM,卡格,Cag1、Cag3和CagT。在这些因素中,CagM和CagE表达连续下调，用亚硒酸钠诱导2小时后进一步下调。此外，CagT表达在第3个周期（6d）前上调，第5个周期后显著下调。Cag1和Cag3表达上调和下调，分别,但是在第5个周期没有观察到明显的变化。用经过亚硒酸钠诱导的减毒株感染C57BL/6A小鼠。幽门螺杆菌在胃中定植的程度增加；然而，亚硒酸钠还在幽门螺杆菌感染小鼠的胃粘膜中诱导轻度炎症反应，H.pylori的细胞粘附能力明显减弱。
结论:这些结果表明幽门螺杆菌在第10天的亚硒酸钠处理后显示出毒力减弱。亚硒酸钠是一种低毒性化合物，具有很强的稳定性，可以降低幽门螺杆菌的细胞粘附能力，从而减轻对胃粘膜的炎症损伤。
