ArticleMedicine2026
Immune-related core gene identification in irritable bowel syndrome and prediction of regulatory traditional Chinese medicines.
Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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8 authors.
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Abstract
Immune dysregulation is increasingly recognized as an important contributor to the pathophysiology of irritable bowel syndrome (IBS). This study aimed to identify immune-related core genes in IBS and predict potential regulatory traditional Chinese medicines (TCMs). Two IBS-related Gene Expression Omnibus datasets were integrated and analyzed to identify differentially expressed genes (DEGs). Functional enrichment, immune cell infiltration profiling, and intersection with ImmPort immune-related genes were performed. Core genes were selected through 3 machine-learning algorithms, and potential TCMs were predicted using the Coremine Medical database. A total of 95 DEGs were identified, including 56 upregulated and 39 downregulated genes. Enrichment analyses indicated involvement in muscle system processes, membrane-associated structures, and peptidase inhibitor activity, with significant enrichment in the neuroactive ligand-receptor interaction pathway. Immune infiltration analysis showed increased M2 macrophages, resting natural killer cells, resting dendritic cells, and activated mast cells in IBS samples. Seven immune-related DEGs were obtained, among which LEFTY1, SLPI, and INSL5 were consistently recognized as core genes across all machine-learning approaches. These genes exhibited distinct immune regulatory relevance. Five TCMs: Drynaria fortunei, Crataegus pinnatifida, Houttuynia cordata, Poria cocos, and Bubalus bubalis horn were predicted as potential therapeutic agents targeting the core genes. LEFTY1, SLPI, and INSL5 represent key immune-related genes in IBS and may contribute to its immune regulatory mechanisms. The predicted TCMs provide potential candidates for further validation in IBS management.
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