Authors
Yonglu Li, Chen Yang, Lujing Li, Miaolei Zhang, Yitao Chen, Jiayi Shi, Huiqian Han, Han Xu, Qing Gu
Published in
Food & function. Aug 14, 2026. Epub Aug 14, 2026.
Abstract
The overgrowth of Desulfovibrio has been increasingly recognized as a hallmark of dysbiosis in certain inflammatory bowel disease (IBD) settings. This pathobiont actively secretes excessive hydrogen sulfide (H2S) via sulfate reduction, which, combined with impaired host detoxification, severely disrupts intestinal sulfur homeostasis and drives mucosal damage. However, conventional therapeutics fail to concurrently address this ecological metabolic imbalance. Here, we demonstrate that L. brevis ZFM820 effectively modulates intestinal ecological sulfur homeostasis to alleviate Desulfovibrio-driven colitis. The probiotic secretes phenyllactic acid (PLA) to inhibit the pathogenic sulfate-reduction pathway of Desulfovibrio, halting toxic H2S production. Concurrently, viable ZFM820 promotes a specific ecological shift characterized by the expansion of endogenous Lacrimispora, facilitating in situ butyrate accumulation. This elevated Lacrimispora-driven butyrate significantly upregulates host epithelial sulfide-detoxifying enzymes (SQR and TST), thereby accelerating luminal H2S clearance, rescuing mitochondrial respiration, and restoring barrier integrity. Neither PLA nor butyrate conferred intestinal protection in isolation, highlighting that only viable L. brevis ZFM820 can integrate these complementary activities within the gut ecosystem to achieve therapeutic efficacy. Collectively, the findings highlight that actively coordinating both sides of intestinal sulfur homeostasis represents an effective and targeted strategy for managing pathobiont-associated intestinal diseases.
PMID:
42596741
Bibliographic data and abstract were imported from PubMed on 14 Aug 2026.
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