ArticleBarrier immunity2026
Intestinal epithelial memory: from inflammatory imprinting to metabolite-shaped immune tolerance.
Article in Barrier immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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Authors and funding
3 authors.
Funding
Abstract
Intestinal epithelial cells are rapidly renewing barrier cells that maintain compartmentalization between the luminal environment and the mucosal immune system through epithelial transport, antimicrobial defense, secretory programs, and cytokine-mediated communication. Emerging evidence suggests that the intestinal epithelium can also retain durable imprints of prior inflammatory, microbial, or metabolic exposures. We refer to this phenomenon as intestinal epithelial memory. This form of memory is likely encoded within stem and progenitor compartments through persistent changes in chromatin accessibility, transcriptional responsiveness, lineage specification, and cellular metabolism. In inflammatory bowel disease, epithelial memory may help explain persistent barrier dysfunction, relapse-prone mucosa, and incomplete epithelial recovery after apparent inflammatory resolution. Human organoid studies show that intestinal stem cells from previously inflamed ulcerative colitis mucosa retain chromatin-based inflammatory memory. Mouse colitis models further show that long-lasting epigenetic imprints in colonic stem cells can generate repair-primed states that promote tumor growth after oncogenic mutation. Microbiota-derived metabolites may represent another class of epithelial memory-shaping cues. This possibility is exemplified by emerging evidence that butyrate can induce sustained epithelial metabolic and epigenetic programs that influence downstream IL-10
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