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ORIGINAL RESEARCH article

Front. Microbiol.

Sec. Food Microbiology

Volume 16 - 2025 | doi: 10.3389/fmicb.2025.1643172

sodA modulates in vitro and in vivo virulence of Yersinia enterocolitica

Provisionally accepted
Yingying  ZhangYingying Zhang1*Yan  MaYan Ma2Xiaodong  XiaXiaodong Xia3Hao  LiHao Li4Jin  TongJin Tong3Xinru  MengXinru Meng3Xing  LiuXing Liu3Xuan  YangXuan Yang3Ruixue  XieRuixue Xie5Li  LiLi Li6*
  • 1College of Life Science and Medicine, Northwest University, Xi'an, China
  • 2School of Biological and Food Processing Engineering, Huanghuai University, Zhumadian, China
  • 3College of Food Science and Engineering, Northwest A&F University, Yangling, China
  • 4College of Life Sceince and Medicine, Northwest University, Xi'an, China
  • 5College of Life Sciences and Medicine, Northwest University, Xi'an, China
  • 6Department of General Surgery, Second Affiliated Hospital of Anhui Medical University, Hefei, China

The final, formatted version of the article will be published soon.

Yersinia enterocolitica, a Gram-negative bacterium, is a major cause of gastroenteritis and can also lead to more severe systemic infections, particularly in immunocompromised individuals. The ability to evade immune responses, invade and survive within host tissues, and proliferate under oxidative stress conditions contributes to its pathogenicity. This study investigates the impact of the gene sodA, encoding manganese-dependent superoxide dismutase (Mn-SOD), on the virulence, colonization, and host immune response of Y. enterocolitica using knockout and complementation strains. The ΔsodA mutants significantly reduced the bacterial adhesion to and invasion of epithelial cells, impaired the intracellular survival of bacteria within macrophages, and decreased the bacterial colonization of the ileum and colon in a mouse model. Compared to the WT strain, these mutants also triggered a weaker inflammatory response, as indicated by lower expression levels of key pro-inflammatory genes such as IL-1β, TNF-α, and inflmmation-related protein NF-κB p65. Complementation of sodA restored these functions, confirming its essential role in virulence and modulation of host immunity. Our findings highlight the critical role of sodA to the survival and virulence of Y. enterocolitica, offering insights into potential therapeutic targets for managing its infections.

Keywords: Yersinia enterocolitica, SodA gene, Pathogenesis, Reactive OxygenSpecies, immune response

Received: 08 Jun 2025; Accepted: 27 Aug 2025.

Copyright: © 2025 Zhang, Ma, Xia, Li, Tong, Meng, Liu, Yang, Xie and Li. 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:
Yingying Zhang, College of Life Science and Medicine, Northwest University, Xi'an, China
Li Li, Department of General Surgery, Second Affiliated Hospital of Anhui Medical University, Hefei, China

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