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Peer-reviewedCC BYMicroorganisms

Gut-to-Liver Escape of Viable Streptococcus salivarius Fuels Alcoholic Liver Disease via Fn14-Dependent NF-κB Signaling.

  • Ranran Zhao1,2
  • Xinqian Gao2,3
  • Shuaiyi Liang3,4
  • Jiegang Huang1,2
  • Zuming Ruan5
  • Zongmao Li6
  • Guangkun Zhang2,3
  • Ping Cui2,3
  • Li Ye1,2,3
  • Hui Chen6
6 affiliations
  1. 1School of Public Health, Guangxi Medical University, Nanning 530021, China.
  2. 2Guangxi Key Laboratory of AIDS Prevention and Treatment, Guangxi Medical University, Nanning 530021, China.
  3. 3Life Sciences Institute, Guangxi Medical University, Nanning 530021, China.
  4. 4Collaborative Innovation Centre of Regenerative Medicine and Medical BioResource Development and Application Co-Constructed by the Province and Ministry, Nanning 530021, China.
  5. 5Department of Gastroenterology, Minzu Hospital of Guangxi Zhuang Autonomous Region, Nanning 530001, China.
  6. 6Department of Geriatric Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
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Abstract

Gut microbial dysbiosis contributes to alcoholic liver disease (ALD), but the pathogenic bacteria and mechanisms remain unclear. We investigated the role of Streptococcus salivarius (S. salivarius) in ALD mice using a modified 12-week NIAAA chronic-plus-binge ethanol regimen with oral gavage. S. salivarius aggravated hepatic steatosis, inflammation, fibrosis, and serum ALT elevation, while impairing colonic mucus and tight-junction integrity. Viable bacteria translocated from the gut to the liver. Integrated hepatic metabolomics and transcriptomics revealed disturbances in bile acid, glycerophospholipid, and choline metabolism and upregulation of Tnfrsf12a, encoding Fn14. S. salivarius activated NF-κB signaling without altering TLR2 or TLR4 abundance. Fn14 silencing or NF-κB inhibition attenuated the inflammatory response in vitro. Thus, our findings suggest that S. salivarius may contribute to ALD progression by impairing the intestinal barrier, translocating to the liver, and activating Fn14-dependent NF-κB signaling. The gut-liver translocation pathway and Fn14/NF-κB axis may represent therapeutic targets for ALD.

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Cite

BibTeXRIS
BibTeX
@article{zhao2026guttoliver,
  title = {{Gut-to-Liver Escape of Viable Streptococcus salivarius Fuels Alcoholic Liver Disease via Fn14-Dependent NF-κB Signaling.}},
  author = {Ranran Zhao and Xinqian Gao and Shuaiyi Liang and Jiegang Huang and Zuming Ruan and Zongmao Li and Guangkun Zhang and Ping Cui and Li Ye and Hui Chen},
  journal = {Microorganisms},
  year = {2026},
  month = oct,
  doi = {10.3390/microorganisms14102297},
  url = {https://europepmc.org/article/MED/42943537},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Gut-to-Liver Escape of Viable Streptococcus salivarius Fuels Alcoholic Liver Disease via Fn14-Dependent NF-κB Signaling.
AU  - Ranran Zhao
AU  - Xinqian Gao
AU  - Shuaiyi Liang
AU  - Jiegang Huang
AU  - Zuming Ruan
AU  - Zongmao Li
AU  - Guangkun Zhang
AU  - Ping Cui
AU  - Li Ye
AU  - Hui Chen
PY  - 2026
DA  - 2026/10/09
JO  - Microorganisms
DO  - 10.3390/microorganisms14102297
UR  - https://europepmc.org/article/MED/42943537
AB  - Gut microbial dysbiosis contributes to alcoholic liver disease (ALD), but the pathogenic bacteria and mechanisms remain unclear. We investigated the role of Streptococcus salivarius (S. salivarius) in ALD mice using a modified 12-week NIAAA chronic-plus-binge ethanol regimen with oral gavage. S. salivarius aggravated hepatic steatosis, inflammation, fibrosis, and serum ALT elevation, while impairing colonic mucus and tight-junction integrity. Viable bacteria translocated from the gut to the liver. Integrated hepatic metabolomics and transcriptomics revealed disturbances in bile acid, glycerophospholipid, and choline metabolism and upregulation of Tnfrsf12a, encoding Fn14. S. salivarius activated NF-κB signaling without altering TLR2 or TLR4 abundance. Fn14 silencing or NF-κB inhibition attenuated the inflammatory response in vitro. Thus, our findings suggest that S. salivarius may contribute to ALD progression by impairing the intestinal barrier, translocating to the liver, and activating Fn14-dependent NF-κB signaling. The gut-liver translocation pathway and Fn14/NF-κB axis may represent therapeutic targets for ALD.
SN  - 2076-2607
ER  -