Biotics-based modulation of gastric precancerous states: microbial, metabolic, and epithelial mechanisms
- 1School of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine
- 2Affiliated Zigong Hospital of Chengdu University of Traditional Chinese Medicine
Abstract
Gastric precancerous states are important intermediate stages in gastric carcinogenesis, yet strategies that directly modify their persistent biological drivers remain limited. Current management mainly includes Helicobacter pylori eradication, endoscopic surveillance, and mucosal protective strategies. Biotics, including probiotics, synbiotics, postbiotics, and next-generation microbial products, have been investigated as potential strategies to modulate persistent microbial, metabolic, inflammatory, and barrier alterations. However, existing evidence derives from studies of H. pylori -associated gastritis and gastric precancerous lesions, as well as related gastric cancer and gastrointestinal models, making it important to distinguish direct evidence from findings in related disease contexts. This review examines evidence for biotic modulation of microbial homeostasis, metabolic and postbiotic signaling, immune and barrier function, and host–microbiota interactions across anatomical compartments during gastric precancerous progression. Current evidence is concentrated largely in H. pylori -associated gastritis, where biotics have been reported to influence microbial composition, inflammatory signaling, metabolic profiles, and barrier function, whereas direct evidence in established atrophy, intestinal metaplasia, and dysplasia remains limited. These findings support further investigation of biotics as strategies for risk modification and homeostatic support rather than as substitutes for established clinical management. Future studies will require better standardization of strains, formulations, dosage, and treatment duration, together with clearly defined histological outcomes and long-term clinical endpoints.
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BibTeX
@article{li2026bioticsbased,
title = {{Biotics-based modulation of gastric precancerous states: microbial, metabolic, and epithelial mechanisms}},
author = {Xi Li and Jian Ma and Gaoyan Shen and Rui Liu and Yun Wang and Jiajun Zhang and Yinling Guo and Xiaoying Hao},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1927527},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1927527/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Biotics-based modulation of gastric precancerous states: microbial, metabolic, and epithelial mechanisms
AU - Xi Li
AU - Jian Ma
AU - Gaoyan Shen
AU - Rui Liu
AU - Yun Wang
AU - Jiajun Zhang
AU - Yinling Guo
AU - Xiaoying Hao
PY - 2026
DA - 2026/10/07
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1927527
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1927527/full
AB - Gastric precancerous states are important intermediate stages in gastric carcinogenesis, yet strategies that directly modify their persistent biological drivers remain limited. Current management mainly includes Helicobacter pylori eradication, endoscopic surveillance, and mucosal protective strategies. Biotics, including probiotics, synbiotics, postbiotics, and next-generation microbial products, have been investigated as potential strategies to modulate persistent microbial, metabolic, inflammatory, and barrier alterations. However, existing evidence derives from studies of H. pylori -associated gastritis and gastric precancerous lesions, as well as related gastric cancer and gastrointestinal models, making it important to distinguish direct evidence from findings in related disease contexts. This review examines evidence for biotic modulation of microbial homeostasis, metabolic and postbiotic signaling, immune and barrier function, and host–microbiota interactions across anatomical compartments during gastric precancerous progression. Current evidence is concentrated largely in H. pylori -associated gastritis, where biotics have been reported to influence microbial composition, inflammatory signaling, metabolic profiles, and barrier function, whereas direct evidence in established atrophy, intestinal metaplasia, and dysplasia remains limited. These findings support further investigation of biotics as strategies for risk modification and homeostatic support rather than as substitutes for established clinical management. Future studies will require better standardization of strains, formulations, dosage, and treatment duration, together with clearly defined histological outcomes and long-term clinical endpoints.
SN - 1664-3224
ER -