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<p>Inflammatory Bowel Disease (IBD) is a chronic inflammatory intestinal disorder with complex etiology, closely associated with gut microbiota dysbiosis. This study demonstrates that <i>Eubacterium rectale</i> (<i>ER</i>), a beneficial commensal bacterium, alleviates dextran sulfate sodium (DSS)-induced colitis in mice, as evidenced by improved clinical symptoms, restored intestinal barrier integrity, and reduced pro-inflammatory cytokine levels. Mechanistic investigations revealed that <i>ER</i> specifically upregulates the expression of glutaminase 2 (GLS2), ameliorates DSS-induced disturbances in glutamine (Gln) metabolism within intestinal epithelial cells, and subsequently inhibits the NF-κB signaling pathway to exert anti-inflammatory effects. Further validation showed that GLS2 deficiency abolishes the anti-inflammatory effects of <i>ER</i>. Collectively, this work identifies a therapeutically relevant mechanism: <i>ER</i> mitigates colitis via the GLS2/NF-κB axis. These insights pave the way for developing <i>ER</i>-derived live biotherapeutic products for IBD.</p>

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Eubacterium rectale Mitigates Inflammatory Bowel Disease via Modulation of Glutamine Metabolism Through the GLS2 and NF-κB Pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月26日

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  • Lu Han,
  • Yiyi Jin,
  • Wen Lin,
  • Zide Liu,
  • Chunyan Zeng,
  • Youxiang Chen

摘要

Inflammatory Bowel Disease (IBD) is a chronic inflammatory intestinal disorder with complex etiology, closely associated with gut microbiota dysbiosis. This study demonstrates that Eubacterium rectale (ER), a beneficial commensal bacterium, alleviates dextran sulfate sodium (DSS)-induced colitis in mice, as evidenced by improved clinical symptoms, restored intestinal barrier integrity, and reduced pro-inflammatory cytokine levels. Mechanistic investigations revealed that ER specifically upregulates the expression of glutaminase 2 (GLS2), ameliorates DSS-induced disturbances in glutamine (Gln) metabolism within intestinal epithelial cells, and subsequently inhibits the NF-κB signaling pathway to exert anti-inflammatory effects. Further validation showed that GLS2 deficiency abolishes the anti-inflammatory effects of ER. Collectively, this work identifies a therapeutically relevant mechanism: ER mitigates colitis via the GLS2/NF-κB axis. These insights pave the way for developing ER-derived live biotherapeutic products for IBD.