Exploring the molecular mechanism of Crohn's disease and rheumatoid arthritis: a bioinformatics and functional analysis approach.

BACKGROUND

Crohn's disease (CD) and rheumatoid arthritis (RA) are autoimmune diseases. CD is known to be closely associated with RA. However, the mechanisms underlying these relationships remain unclear. This study aimed to explore the common genetic features and potential molecular mechanisms of CD and RA.

METHODS

Microarray data of CD and RA in the Gene Expression Omnibus database were downloaded. Weighted gene coexpression network analysis (WGCNA) was used to identify the coexpression modules related to CD and RA. The shared genes existing in CD and RA were subjected to gene ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis using R software. The results were validated by differentially expressed genes (DEGs) analysis to enrich for common differential genes and unique genes in CD and RA. Based on CD-RA common hub genes, we explored the feasibility of developing new gene-antibody coupled targeted drugs for the treatment of CD-RA.

RESULTS

Enrichment analysis of gene modules identified through WGCNA revealed disease pathway models suggesting potential mechanisms of RA secondary to CD. Furthermore, we identified key shared pathogenic genes between CD and RA, such as S100P and IL2RB that may be important targets for the treatment of both diseases.

CONCLUSION

The study is the first to reveal the key pathways underlying the shared pathogenesis of CD and RA, identify novel candidate genes that could serve as biomarkers or potential therapeutic targets. Finally, we propose new ideas for the development of gene-antibody coupled targeted drugs.