ArticleGastroenterology2026
Harmonized Metagenomic Signatures of the Gut Microbiome Reveal Robust Species, Functions, and Strain Links to Inflammatory Bowel Disease.
Article in Gastroenterology, 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.
- Preventive Effects of Fermented Yak Milk-DerivedFoods (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
BACKGROUND &
aimsCoupled with well-characterized host genetic and environmental risk factors, alterations of gut microbial communities contribute to risk and severity of inflammatory bowel disease (IBD) and its subtypes, Crohn's disease (CD) and ulcerative colitis (UC). In a rapidly advancing field in which diverse multinational cohorts and molecular methods have been created, highly resolved microbial traits such as protein function and strain genetics can now be investigated through meta-analysis.
methodsWe integrated 2371 stool metagenomes from 542 individuals with IBD and their referent counterparts from the United States, Canada, and Europe, using all 7 IBD cohorts in the Human Microbiome Bioactives Resource, which we interrogated using taxonomic, functional, and strain profiling.
resultsWe systematically identified the mass expansion of proinflammatory, oral-predominant taxa in the IBD gut, such as Veillonella and Streptococcus spp. We also accurately discriminate CD from UC, a clinically challenging problem, using highly resolved microbial strain genetics (area under the curve = 0.69). Further, we observed disease-specific shifts in carbohydrate metabolism, a likely consequence of small bowel dysfunction in CD, but not UC, as well as perturbations in mucin use, increased microbial virulence and invasion cassettes, and loss of carnitine degradation pathways in IBD. Finally, we observed novel and significant differences in the gene carriage among both IBD- and non-IBD-associated taxa, suggesting that strain-specific functional variation may contribute to pathogenesis and disease-related bacterial fitness.
conclusionsMicrobial clades responsible for IBD-linked dysbiosis are not uniform, and their functionality in IBD and CD/UC subsets are driven by species and strain lineage-specific variants.
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