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Peer-reviewedCC BYVirulence

Subverting colonization resistance: Salmonella pathogenesis at the interface of microbiota, metabolism and inflammasome.

  • Zhixin Gao1,2,3
  • Zheng Li1,2,3,4
  • Jianyang Cui1,2,3,4
  • Qing Zhang1,2,3,4
  • Yanyan Jia1,2,3,4
  • Ke Ding1,2,3,4
  • Ke Shang1,2,3,4
  • Songbiao Chen1,2,3,4
4 affiliations
  1. 1Laboratory of Functional Microbiology and Animal Health, College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, P.R. China.
  2. 2Luoyang Key Laboratory of Live Carrier Biomaterial and Animal Disease Prevention and Control, Henan University of Science and Technology, Luoyang, P.R. China.
  3. 3The Key Lab of Animal Disease and Public Health, Henan University of Science and Technology, Luoyang, P.R. China.
  4. 4Ministry of Education Key Laboratory for Animal Pathogens and Biosafety, Zhengzhou, P.R.China.
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Abstract

The intestinal tract is a key immune organ and microecological system, where colonization resistance (CR) mediated by gut microbiota prevents pathogen invasion. Salmonella disrupts CR via type VI and type III secretion systems (T6SS/T3SS), inducing dysbiosis, inflammasome-driven inflammation, and intestinal barrier damage. This creates a self-reinforcing cycle:dysbiosis alters microbial metabolites, sustains inflammation, and enhances pathogen fitness, favoring chronic infection. This review integrates molecular mechanisms of microbiota disruption, inflammasome activation, and metabolic imbalance to explain how Salmonella overcomes CR. We also highlight microbiota-based countermeasures, including probiotics, natural antimicrobials, and phage therapy, as promising strategies to restore gut homeostasis.

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Cite

BibTeXRIS
BibTeX
@article{gao2026subverting,
  title = {{Subverting colonization resistance: Salmonella pathogenesis at the interface of microbiota, metabolism and inflammasome.}},
  author = {Zhixin Gao and Zheng Li and Jianyang Cui and Qing Zhang and Yanyan Jia and Ke Ding and Ke Shang and Songbiao Chen},
  journal = {Virulence},
  year = {2026},
  month = oct,
  doi = {10.1080/21505594.2026.2745323},
  url = {https://europepmc.org/article/MED/42885908},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Subverting colonization resistance: Salmonella pathogenesis at the interface of microbiota, metabolism and inflammasome.
AU  - Zhixin Gao
AU  - Zheng Li
AU  - Jianyang Cui
AU  - Qing Zhang
AU  - Yanyan Jia
AU  - Ke Ding
AU  - Ke Shang
AU  - Songbiao Chen
PY  - 2026
DA  - 2026/10/16
JO  - Virulence
DO  - 10.1080/21505594.2026.2745323
UR  - https://europepmc.org/article/MED/42885908
AB  - The intestinal tract is a key immune organ and microecological system, where colonization resistance (CR) mediated by gut microbiota prevents pathogen invasion. Salmonella disrupts CR via type VI and type III secretion systems (T6SS/T3SS), inducing dysbiosis, inflammasome-driven inflammation, and intestinal barrier damage. This creates a self-reinforcing cycle:dysbiosis alters microbial metabolites, sustains inflammation, and enhances pathogen fitness, favoring chronic infection. This review integrates molecular mechanisms of microbiota disruption, inflammasome activation, and metabolic imbalance to explain how Salmonella overcomes CR. We also highlight microbiota-based countermeasures, including probiotics, natural antimicrobials, and phage therapy, as promising strategies to restore gut homeostasis.
SN  - 2150-5594
SN  - 2150-5608
ER  -