ArticleJournal of advanced research2026
Gut microbiota dysbiosis transmits deoxynivalenol toxicity and triggers liver inflammation.
Article in Journal of advanced research, 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
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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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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
2 citing papers in PubMed.
- Protective Effects ofBiology · 2026Article
- Mechanistic evidence and assumptions in mycotoxin-gut interaction.Frontiers in fungal biology · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionDeoxynivalenol (DON), a mycotoxin produced by Fusarium species, is known to compromise gut barrier integrity and induce systemic inflammation.
objectivesThis study demonstrates that intestinal microbiota play a central role in DON-induced liver inflammation.
methodsThrough oral exposure and fecal microbiota transplantation (FMT) experiments in mice, we observed that DON disrupts intestinal structure, alters microbial composition, and activates liver inflammation via the TLR4/MyD88/NF-κB pathway.
resultsNotably, liver inflammation was replicated in pseudo-germ-free mice colonized with microbiota from DON-exposed donors, even in the absence of direct DON exposure. Microbial analysis identified Alloprevotella, a mucin-degrading genus associated with increased intestinal permeability, and Pseudomonas, a pathogenic genus enriched in the liver, as key candidate microbial drivers of this effect.
conclusionThese findings underscore that dysbiosis, especially involving specific bacterial genera, can independently trigger liver inflammation, highlighting a microbiota-mediated pathogenic mechanism in mycotoxin toxicity.
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