Bile acid metabolism modulates intestinal immunity involved in ulcerative colitis progression.

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.