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Background <p>Intestinal metaplasia (IM) is a key precancerous lesion connecting chronic atrophic gastritis and gastric cancer in the Correa cascade, and its risk of progression has significant individual heterogeneity. A potential explanatory framework for this heterogeneity involves interactions between gastric microbiota imbalance and host epigenetic remodeling. Current research needs to clarify the relationship between microbial community stratification and IM reversibility, particularly whether high-risk microbial signatures and putative epigenetic “silencer locking” states are associated with IM regression or persistence.</p> Method <p>This hypothesis-driven narrative review synthesizes representative findings from metagenomic, metabolomic, transcriptomic, and epigenomic studies to develop a conceptual framework for how interactions between Helicobacter pylori (<i>H. pylori</i>), non-<i>H. pylori</i> microorganisms, and host mucosal responses may be associated with the initiation and progression of IM, potentially through microbiota-associated, host-derived, and mixed-origin metabolic signals that converge on epigenetic and transcriptional regulation.</p> Result <p>Available evidence suggests that microbial networks in IM may include potential pro-inflammatory interactions between <i>H. pylori</i> and taxa such as <i>Fusobacterium nucleatum</i> (<i>F. nucleatum</i>), as well as possible protective associations involving beneficial bacteria such as Lactobacillus. Based on this, we propose a three-stage working model, <i>H. pylori</i> initiation, putative microbial network amplification, and silencer remodeling-associated progression, and discuss a candidate intervention framework involving probiotics, miR-185, and Wnt/β-catenin signaling, which should be regarded as a testable hypothesis rather than a clinically validated reversal strategy.</p> Conclusion <p>These findings may provide candidate mechanistic targets and a theoretical basis for future risk stratification, dynamic monitoring, and individualized intervention of IM, pending validation in prospective clinical studies.</p>

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From microbial dysbiosis to putative epigenetic locking: a hypothesis-driven framework for the pathogenesis and future therapeutic perspectives of gastric intestinal metaplasia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • Yingyue Sheng,
  • Chaosheng Yan,
  • Yuzhe Yin,
  • Zhipeng Zeng,
  • Xinyu Pei,
  • Chenyu Ma,
  • Jingjing Rao,
  • Haowen Sun,
  • Yuzheng Xue

摘要

Background

Intestinal metaplasia (IM) is a key precancerous lesion connecting chronic atrophic gastritis and gastric cancer in the Correa cascade, and its risk of progression has significant individual heterogeneity. A potential explanatory framework for this heterogeneity involves interactions between gastric microbiota imbalance and host epigenetic remodeling. Current research needs to clarify the relationship between microbial community stratification and IM reversibility, particularly whether high-risk microbial signatures and putative epigenetic “silencer locking” states are associated with IM regression or persistence.

Method

This hypothesis-driven narrative review synthesizes representative findings from metagenomic, metabolomic, transcriptomic, and epigenomic studies to develop a conceptual framework for how interactions between Helicobacter pylori (H. pylori), non-H. pylori microorganisms, and host mucosal responses may be associated with the initiation and progression of IM, potentially through microbiota-associated, host-derived, and mixed-origin metabolic signals that converge on epigenetic and transcriptional regulation.

Result

Available evidence suggests that microbial networks in IM may include potential pro-inflammatory interactions between H. pylori and taxa such as Fusobacterium nucleatum (F. nucleatum), as well as possible protective associations involving beneficial bacteria such as Lactobacillus. Based on this, we propose a three-stage working model, H. pylori initiation, putative microbial network amplification, and silencer remodeling-associated progression, and discuss a candidate intervention framework involving probiotics, miR-185, and Wnt/β-catenin signaling, which should be regarded as a testable hypothesis rather than a clinically validated reversal strategy.

Conclusion

These findings may provide candidate mechanistic targets and a theoretical basis for future risk stratification, dynamic monitoring, and individualized intervention of IM, pending validation in prospective clinical studies.