ReviewFrontiers in microbiology2026
Microbial metabolic memory in inflammatory bowel disease: microbiota-derived metabolites, host-microbe reprogramming, and relapse susceptibility.
Review in Frontiers in microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease (IBD) is increasingly recognized as a disorder of disrupted host-microbe metabolic communication rather than a consequence of microbial dysbiosis alone. Gut microbiota-derived metabolites, including short-chain fatty acids, tryptophan derivatives, bile acid metabolites, polyamines, lactate, succinate, and trimethylamine N-oxide, act as functional mediators linking microbial ecological changes to epithelial barrier integrity, mucosal immune activation, inflammatory amplification, and tissue repair. However, most existing discussions have focused on individual metabolites or isolated immune pathways, leaving the dynamic and disease-stage-specific nature of microbial metabolic remodeling insufficiently defined. In this review, we reframe IBD pathogenesis from the perspective of microbial metabolic memory, emphasizing how persistent alterations in microbial metabolic output may imprint epithelial and immune cell responses even after clinical remission. We summarize how protective metabolite depletion and proinflammatory metabolite accumulation contribute to immune tolerance breakdown, barrier dysfunction, inflammatory propagation, extraintestinal immune manifestations, and relapse susceptibility. We further discuss how mucosal inflammation reciprocally reshapes microbial niches, oxygen tension, nutrient availability, and metabolic pathway activity, thereby establishing self-reinforcing host-microbe feedback loops. Finally, we evaluate emerging therapeutic strategies, including metabolite supplementation, blockade of proinflammatory metabolic signaling, microbiota-based metabolic remodeling, engineered probiotics, and metabolomics-guided precision interventions. This metabolic-memory framework may provide a more integrated basis for understanding IBD recurrence and for developing microbiota-targeted strategies aimed at restoring durable intestinal homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.