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World J Gastroenterol. Jan 7, 2024; 30(1): 91-107
Published online Jan 7, 2024. doi: 10.3748/wjg.v30.i1.91
Mechanistic research: Selenium regulates virulence factors, reducing adhesion ability and inflammatory damage of Helicobacter pylori
Chun Qin, Gan-Rong Huang, Ai-Xing Guan, Wen-Ting Zhou, Hao Chen, Pei-Pei Luo, Xian-Ke Luo, Yan-Qiang Huang, Zan-Song Huang
Chun Qin, Gan-Rong Huang, Ai-Xing Guan, Wen-Ting Zhou, Yan-Qiang Huang, Zan-Song Huang, Guangxi Technology Innovation Cooperation Base of Prevention and Control Pathogenic Microbes with Drug Resistance, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Chun Qin, Ai-Xing Guan, Zan-Song Huang, Department of Digestive Diseases, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Gan-Rong Huang, Wen-Ting Zhou, Yan-Qiang Huang, Key Laboratory of the Prevention and Treatment of Drug Resistant Microbial Infecting, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Hao Chen, Department of Pathology, Wannan Medical College, Wuhu 241002, Anhui Province, China
Pei-Pei Luo, Department of Gastroenterology, Wujin People’s Hospital affiliated to Jiangsu University, Changzhou 213004, Jiangsu Province, China
Xian-Ke Luo, Department of Gastroenterology, Guangzhou Liwan District People's Hospital, Guangzhou 510370, Guangdong Province, China
Co-corresponding authors: Yan-Qiang Huang and Zan-song Huang.
Author contributions: Qin C and Huang GR were responsible for the experimental research, reviewed the literature, and drafted the manuscript; Qin C and Huang GR contributed equally to this study; Guan AX, Zhou WT, Chen H, Luo PP, and Luo XK were responsible for writing, reviewing, and editing the study; All authors were involved in the critical review of the results and have contributed to, read, and approved the final manuscript; Huang YQ and Huang ZS contributed equally to this work as co-corresponding authors. The reasons for designating Huang YQ and Huang ZS as co-corresponding authors are threefold. First, the research was performed as a collaborative effort, and the designation of co-corresponding authorship accurately reflects the distribution of responsibilities and burdens associated with the time and effort required to complete the study and the resultant paper. This also ensures effective communication and management of post-submission matters, ultimately enhancing the paper’s quality and reliability. Second, the overall research team encompassed authors with a variety of expertise and skills from different fields, and the designation of co-corresponding authors best reflects this diversity. This also promotes the most comprehensive and in-depth examination of the research topic, ultimately enriching readers' understanding by offering various expert perspectives. Third, Huang YQ and Huang ZS contributed efforts of equal substance throughout the research process. The choice of these researchers as co-corresponding authors acknowledges and respects this equal contribution, while recognizing the spirit of teamwork and collaboration of this study. In summary, we believe that designating Huang YQ and Huang ZS as co-corresponding authors of is fitting for our manuscript as it accurately reflects our team's collaborative spirit, equal contributions, and diversity.
Supported by National Natural Science Foundation of China, No. 32060018 and No. 32360035; Through Special Fund Projects for Guide Local Science and Technology Development by the China Government, No. GUIKEZY20198004; Anhui Provincial Natural Science Foundation, No. 2308085QH245; the Natural Science Foundation of the Anhui Higher Education Institutions of China, No. 2023AH040261; and Changzhou Science and Technology Project Fund, No. CJ20210012.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Youjiang Medical University for Nationalities Institutional Review Board.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE Guidelines, and the manuscript was prepared and revised according to the ARRIVE Guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
https://creativecommons.org/Licenses/by-nc/4.0/ Corresponding author: Zan-Song Huang, Professor, Guangxi Technology Innovation Cooperation Base of Prevention and Control Pathogenic Microbes With Drug Resistance, Youjiang Medical University for Nationalities, No. 98 Urban-Rural Road, Baise 533000, Guangxi Zhuang Autonomous Region, China.
1019846481@qq.com
Received: October 26, 2023
Peer-review started: October 26, 2023
First decision: November 13, 2023
Revised: November 22, 2023
Accepted: December 13, 2023
Article in press: December 13, 2023
Published online: January 7, 2024
Processing time: 72 Days and 9.1 Hours
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.
AIM
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.
CONCLUSION
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.
Core Tip: The situation caused by Helicobacter pylori drug resistance is critical. Selenium is one of the trace elements in the human body, and its content in the stomach is related to the degree of H. pylori infection. Initial studies have shown that sodium selenite has inhibitory effects on H. pylori, so we further investigated the mechanism of action of sodium selenite on H. pylori. This study provides an experimental basis for use of the trace element selenium in the treatment of H. pylori infection.
