Screening for central targets and the commonalities between rheumatoid arthritis and idiopathic pulmonary fibrosis based on bioinformatics

Abstract

Abstract Background: Despite the mounting proof that those suffering from rheumatoid arthritis (RA) are more likely to experience idiopathic pulmonary fibrosis (IPF), The precise molecular processes that underlie this correlation are yet to be fully comprehended. Hence, the objective of this research was to investigate the molecular workings of RA in conjunction with IPF. Methods: The researchers obtained four datasets from the Gene Expression Omnibus (GEO) database, adhering to a rigorous set of inclusion and exclusion standards. Bioinformatics analyses were performed to identify common differentially expressed genes (DEGs) and hub genes, including functional annotation, co-expression analysis and construction of regulatory TF-mRNA-miRNA networks. The CIBERSORT algorithm was employed to evaluate the association between hub genes and infiltrating immune cells in RA and IPF, in order to examine and contrast immune infiltration. Results: Out of the 153 DEGs that were screened between GSE53845 and GSE55235, the GO and KEGG functional analyses showed that the pathogenesis of these genes may be related to immune factors. After constructing a protein-protein interaction (PPI) network, four hub genes (THY1, CD19, CCL5 and CD8A) were identified, and further bioinformatic analysis revealed that hub genes are involved in cell migration, cytokine activity, chemokine response and chemokine binding. Ultimately, the CIBERSORT-based algorithm detected three immune cells that were infiltrating both RA and IPF, namely CD4+ memory T cells that were upregulated, M1 macrophages, and CD8+ T cells that overlapped. The presence of THY1, CD8A, CCL5, and CD19 was linked to memory activated CD4+ T cells and CD8+ T cells when immune cells were associated with hub genes. Conclusions: This study uncovered that THY1, CD19, CCL5 and CD8A may serve as commonly diagnostic biomarkers for RA and IPF. CD4+ memory T cells, M1 macrophages and CD8+ T cells are involved in the development of RA and IPF. Targeting these cells and targets may be the therapeutic direction of future research into RA-IPF comorbidity.