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<p>Gut microbiota dysbiosis and immune dysregulation are closely associated with the development of colorectal cancer. Identifying the mechanistic links among specific microbial species, metabolites, and immune responses is crucial for uncovering novel insights into its pathogenesis. Here we show, through metagenomic and metabolomic analyses of clinical cohorts, that <i>Fusobacterium periodonticum</i> is significantly enriched in colorectal cancer patients and strongly correlated with elevated decanoic acid levels. Single-cell transcriptomic results further reveal tissue-specific neutrophil enrichment in colorectal cancer tissues, characterized by high <i>CXCL8</i> expression and activation of neutrophil-related immune pathways. Cellular experiments demonstrate that decanoic acid induces late apoptosis/necrosis of neutrophils, enhances their chemotaxis through a pertussis toxin-sensitive G-protein-dependent mechanism, and upregulates genes involved in leukocyte migration and tumorigenesis. Mouse models further confirm that <i>F. periodonticum</i> colonization increases intestinal dysplasia and decanoic acid levels, and that decanoic acid intervention promotes tumor progression by facilitating neutrophil infiltration and modulating the local immune microenvironment. Our study reveals an important role of <i>F. periodonticum</i> in colorectal tumorigenesis via decanoic acid-medicated neutrophil chemotaxis, providing mechanistic insights into the pathogenesis of colorectal cancer.</p>

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Fusobacterium periodonticum promotes colorectal tumorigenesis via decanoic acid-driven neutrophil chemotaxis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月24日

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  • Xinmiao Jia,
  • Lingjuan Jiang,
  • Yiyi Gong,
  • Xiaobing Chu,
  • Wei Yu,
  • Juan Du,
  • Jingjia Zhang,
  • Xuesong Shang,
  • Peipei Wang,
  • Jing Wang,
  • Yaqian Li,
  • Zheng Wang,
  • Runing Zhou,
  • Zongping Li,
  • Ying Zhu,
  • Bin Wu,
  • Jingnan Li,
  • Qiwen Yang

摘要

Gut microbiota dysbiosis and immune dysregulation are closely associated with the development of colorectal cancer. Identifying the mechanistic links among specific microbial species, metabolites, and immune responses is crucial for uncovering novel insights into its pathogenesis. Here we show, through metagenomic and metabolomic analyses of clinical cohorts, that Fusobacterium periodonticum is significantly enriched in colorectal cancer patients and strongly correlated with elevated decanoic acid levels. Single-cell transcriptomic results further reveal tissue-specific neutrophil enrichment in colorectal cancer tissues, characterized by high CXCL8 expression and activation of neutrophil-related immune pathways. Cellular experiments demonstrate that decanoic acid induces late apoptosis/necrosis of neutrophils, enhances their chemotaxis through a pertussis toxin-sensitive G-protein-dependent mechanism, and upregulates genes involved in leukocyte migration and tumorigenesis. Mouse models further confirm that F. periodonticum colonization increases intestinal dysplasia and decanoic acid levels, and that decanoic acid intervention promotes tumor progression by facilitating neutrophil infiltration and modulating the local immune microenvironment. Our study reveals an important role of F. periodonticum in colorectal tumorigenesis via decanoic acid-medicated neutrophil chemotaxis, providing mechanistic insights into the pathogenesis of colorectal cancer.