Genomic Research for Abdominal Pain in Patients with Irritable Bowel Syndrome or Inflammatory Bowel Disease Before and After Mind-Body Intervention

Purpose: Abdominal pain is a hallmark symptom of both inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) and substantially impairs patients’ quality of life. Relaxation response–based mind–body intervention (RR-MBI) has been reported to improve disease-specific outcomes and pain catastrophizing in both disorders, accompanied by whole-blood transcriptomic changes. However, the transcriptional features potentially relevant to abdominal pain before and after RR-MBI in IBS and IBD remain insufficiently explored. In this context, this study aimed to analyze these transcriptional changes and prioritize putative abdominal pain-relevant candidate genes from exploratory differentially expressed gene (DEG) sets. Patients and Methods: Gene expression data (GSE66824) were obtained from the Gene Expression Omnibus (GEO). Whole-blood gene expression profiles were analyzed from 14 IBS and 19 IBD patients, with samples collected before and after a 9-week RR-MBI. Exploratory DEG sets were identified using GEO2R outputs with nominal P < 0.05 and absolute fold-change magnitude (AFC) ≥ 1.2. Functional enrichment analyses were performed using DAVID. Protein–protein interaction (PPI) networks were constructed using STRING and visualized in Cytoscape. Putative abdominal pain-relevant candidate genes were prioritized from exploratory DEG sets within PPI/MCODE modules based on network position, matching module genes to the DisGeNET disease entry “pain”, and targeted pain-related literature annotation. Results: (1) In IBD post-MBI, 649 exploratory DEGs were identified, with enrichment of neurotrophin and TGF-β signaling pathways; MAP3K7, SLC12A2, and FKBP5 were prioritized as candidate genes. (2) In IBS post-MBI, 175 exploratory DEGs were identified, with enrichment of glutamatergic synapse and calcium signaling pathways; network analysis highlighted NTRK2, FKBP5, and AR as candidate genes. (3) At baseline, 836 exploratory DEGs were identified, with enrichment in pathways including p53 signaling and NOD-like receptor signaling; notable prioritized candidate genes included TRAF6 and TNFSF11. Conclusion: Prioritized genes after RR-MBI and in the baseline comparison may represent putative abdominal pain-relevant candidate transcriptional signals in IBS and IBD. These exploratory findings require validation in independent cohorts with matched individual-level pain-related outcomes and functional studies.