ArticleHeliyon2024
Bile acid metabolism modulates intestinal immunity involved in ulcerative colitis progression.
Article in Heliyon, 2024. 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.
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
2 citing papers in PubMed.
- Regulation of PD-1PD-L1 Immune Checkpoints by Gut Microbiota Metabolites and Their Clinical Translational Research: A Review.Immunity, inflammation and disease · 2026Review
- Investigating the molecular mechanisms associated with ulcerative colitis through the application of single-cell combined spatial transcriptome sequencing.Frontiers in immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The bile acids (BA) in the intestine promote inflammation by interacting with immune cells, playing a crucial role in the progression of UC, but the specific mechanism between the two remains elusive. This study aims to explore the relationship between BAMand UC inflammation and determine its potential mechanisms.Firstly, we employed a hybrid approach using Lasso regression and support vector machine (SVM) feature selection in bioinformatics to identify genes linked to UC and BAM. The relationship between these genes and immune infiltration was explored, along with their correlation with immune factors in the Tumor-Immune System Interaction Database (TISIDB) database. Gene Set Enrichment Analysis (GSEA) pathway enrichment analysis was then used to predict signaling pathways associated with key genes in UC. Single-cell data from the GSE13464 dataset was also analyzed. Finally, Five differentially expressed genes (DEGs) related to BAM (APOA1, AMACR, PEX19, CH25H, and AQP9) were significantly upregulated/downregulated in UC immune cells. The expression of important genes in UC tissue was confirmed in the experimental validation section and AQP9, which showed significant differential expression, was chosen for further validation. The results showed that the AQP9 gene may regulate the IFN - γ/JAK signaling axis, thereby promoting CD8+T cell activation. This research has greatly advanced our comprehension of the pathogenesis and underlying mechanism of BAM in immune cells linked to UC.
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Registered trials
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