Exploring Immune Cell Infiltration and Small Molecule Compounds for Ulcerative Colitis Treatment

Area of Science:

• Genomics and Bioinformatics
• Immunology
• Gastroenterology

Background:

• Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease (IBD) with a complex etiology.
• Bioinformatics approaches are increasingly used to understand disease mechanisms.
• Identifying key genes and therapeutic targets is crucial for UC management.

Purpose of the Study:

• To identify crucial differentially expressed genes (DEGs) in UC.
• To explore potential therapeutic agents for UC using bioinformatics.
• To gain insights into the pathogenesis of UC.

Main Methods:

• Downloaded and analyzed colon tissue transcriptome datasets (GSE47908, GSE55306) from the Gene Expression Omnibus (GEO).
• Utilized GEO2R, Gene Set Enrichment Analysis (GSEA), and Weighted Gene Co-expression Network Analysis (WGCNA) to identify DEGs and hub genes.
• Performed Gene Ontology (GO) and KEGG pathway enrichment analyses, STRING/Cytoscape for hub gene analysis, and ImmuCellAI for immune cell infiltration.
• Screened for potential therapeutic compounds using the CMap database.

Main Results:

• Identified 12 hub genes (e.g., CXCL8, IL1β, CXCL1, CCL20) associated with UC pathogenesis.
• GSEA revealed enriched pathways including colorectal cancer and apoptosis.
• Enrichment analyses highlighted key biological processes (inflammatory response, leukocyte activation) and signaling pathways (cytokine-cytokine receptor interactions, IBD).
• Immune cell infiltration analysis indicated altered levels of various T cells and natural killer cells in UC.
• Vorinostat, roxarsone, and wortmannin were identified as potential therapeutic candidates.

Conclusions:

• This study provides novel insights into UC pathogenesis by identifying key genes and pathways.
• The findings support early prediction and prevention strategies for UC.
• Potential therapeutic small molecules were identified, offering new avenues for UC treatment.