ArticleSmall (Weinheim an der Bergstrasse, Germany)2026
Human Colitis-on-Chip Model Reveals Dual Roles of Butyrate in Epithelial and Macrophage Defense Against Candida albicans Tissue Invasion.
Article in Small (Weinheim an der Bergstrasse, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Supplementation ofNutrients · 2026Article
- Microbial metabolic memory in inflammatory bowel disease: microbiota-derived metabolites, host-microbe reprogramming, and relapse susceptibility.Frontiers in microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Microbial dysbiosis in inflammatory bowel disease (IBD) reduces intestinal butyrate levels, compromising epithelial barrier integrity and enabling overgrowth of opportunistic pathogens such as Candida albicans. Here, we present a human immunocompetent colitis-on-chip model (CooC) that mimics key features of inflamed gut mucosa, including DSS-induced epithelial damage and C. albicans tissue invasion. Using this model, we uncover dual protective roles of microbiota-derived butyrate: (i) stabilization of epithelial adherens junctions and promotion of epithelial renewal, thereby restricting fungal invasion; and (ii) modulation of macrophage function to enhance antifungal activity while attenuating inflammasome-mediated inflammation. Butyrate pretreatment preserves barrier function, limits fungal translocation, and promotes macrophage viability through the inhibition of histone deacetylase (HDAC) and the suppression of NLRP3 inflammasome activation. These findings position butyrate as a key metabolite in orchestrating epithelial-immune defense against fungal exacerbation in colitis, supporting its therapeutic and preventive potential in restoring mucosal resilience in IBD.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.