ORIGINAL RESEARCH article
Front. Cell. Infect. Microbiol.
Sec. Molecular Bacterial Pathogenesis
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1659729
This article is part of the Research TopicMechanisms of microbial persistence and strategies to counter themView all 5 articles
Characterization and immunoprotection of thioredoxin reductase TrxB knockout mutant of Salmonella Enteritidis
Provisionally accepted
Siping Zhu1
Lili Wang1Hong Li1Chihuan Li1Xintong Zhu1Chao Ren1Xiaochen Liu1Yulai Dong2Qiumei Shi1
Zhiqiang Zhang1*- 1Hebei Normal University of Science and Technology, Qinhuangdao, China
- 2Weichang Man and Mongolian Autonomous County Xinrui Agricultural Development Ltd, Qinhuangdao, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Background: Salmonella Enteritidis (S. Enteritidis ) is an important zoonotic pathogen that poses a major threat to animals and human health. TrxB, as a key component of the thioredoxin system, is a thioredoxin reductase ubiquitously present in organisms. It is mainly involved in maintaining cellular redox balance, but its role in the pathogenicity of S. Enteritidis remains unclear. Methods: In this study, we generated a trxB-deficient strain from S. Enteritidis C50336 strain to investigate how TrxB affects the biological characteristics and pathogenesis of the bacterium. The virulence of ΔtrxB was assessed by measuring ΔtrxB resistance to environmental stress, biofilm formation ability, motility, adhesion, invasion ability, intracellular survival, LD50, virulence gene expression levels, and in vivo colonization ability. Additionally, the study measured specific IgG antibody levels in mice, lymphocyte proliferation, and the immunoprotective effect of ΔtrxB. Results: We found that deletion of trxB gene did not affect the growth and biochemical properties of the S. Enteritidis strain but significantly reduced its motility, drug resistance, biofilm formation, and tolerance to environmental stress. After trxB knockedout, the adhesion and invasion capacities of S. Enteritidis to Caco-2 cells, along with its proliferation in RAW264.7 cells, were significantly reduced. Additionally, the trxB-deficient strain exhibited significantly lower pathogenicity than the parental strain, evidenced by a more than 100-fold increase in LD50. We also observed a significant decrease in the expression of virulence-related genes in the trxB-knockout mutant. More importantly, immunization with this deletion strain can confer promising protection against challenge with the C50336 strain. Conclusion: These findings indicate that TrxB is a crucial virulence factor in S. Enteritidis, playing critical roles in its pathogenicity.
Keywords: Salmonella enteritidis, TrxB, Gene Deletion, Virulence, Vaccine
Received: 04 Jul 2025; Accepted: 01 Sep 2025.
Copyright: © 2025 Zhu, Wang, Li, Li, Zhu, Ren, Liu, Dong, Shi and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Zhiqiang Zhang, Hebei Normal University of Science and Technology, Qinhuangdao, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.