Source: openalex · Origin: CN · Lu Han, Yiyi Jin, Wen Lin, Zide Liu, Chunyan Zeng · npj Science of Food · 2026-05-26
URL: https://doi.org/10.1038/s41538-026-00876-7
AI rationale (4/5, tier: preliminary): Mouse mechanistic study of commensal bacterium modulating intestinal barrier via metabolic pathway; directly addresses barrier integrity and microbe-host signalling.
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.
