Background • Asthma and chronic obstructive pulmonary disease (COPD) are prevalent respiratory conditions with overlapping pathogenic features such as chronic inflammation.
Primary Study Objective • This study aimed to identify key contributors and pathways that are common to both of these disorders, potentially allowing for the detection of therapeutic targets, particularly for patients with asthma-COPD overlap syndrome.
Methods • Using an integrated transcriptomics approach, eight datasets were analyzed, including two each for COPD and asthma, in both blood and airway epithelial cells. Thereafter, by identifying shared differentially expressed genes between COPD and asthma, protein-protein interaction and miRNA-mRNA regulatory networks were constructed for blood and epithelial cells, and hub genes were determined. Lastly, functional enrichment analysis was conducted to determine the biological functions of the discovered shared protein-protein interaction (PPI) networks.
Results • The construction of shared PPI networks for these two respiratory disorders highlighted key hub genes, including ribosomal proteins and IL-1ß in blood and CTNNB1 in airway epithelial cells. Two members of the miR-30 family, including miR-30a-3p and miR-30e-3p, were discerned as multi-target regulators of hub genes in both networks of blood and airway epithelial cells. Infection-related pathways were substantially enriched, as revealed by functional analysis of shared networks for both blood and airway epithelial cells.
Conclusion • IL-1ß signaling may serve as a potential link between asthma and COPD, since it was identified as a hub gene in the shared network of blood. Likewise, downregulated CTNNB1 was discerned as a key gene in the shared network of airway epithelial samples.
