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Gut microbiome metabolites meet immunometabolism in inflammatory bowel disease
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DOI：10.1016/j.it.2026.06.001.png)
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Abstract
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Inflammatory bowel disease, encompassing Crohn’s disease and ulcerative colitis, represents a group of chronic inflammatory disorders of the gastrointestinal tract that are closely associated with dysregulated host sensing and integration of gut microbiota-derived signals, alongside alterations in microbial composition, functional capacity, and metabolite profiles. Gut microbiota and their metabolites shape immunometabolic programs in intestinal epithelial and resident immune cells, thereby determining cell fate, differentiation, and effector functions, ultimately influencing the initiation and progression of inflammatory bowel disease. The bacterial–mitochondrial endosymbiosis concept highlights that disruption of mitochondrial signaling not only impairs epithelial bioenergetic support but also triggers innate immune activation through mitochondrial damage-associated molecular patterns, contributing to intestinal inflammation. Targeting the gut microbiota–metabolite–immunometabolism axis offers important therapeutic potential and a forward-looking framework for the precision treatment of inflammatory bowel disease.
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