Screening of cytokines-cytokine receptor-associated genes in childhood asthma based on bioinformatics

To develop efficient diagnostic and treatment approaches, gaining an in-depth knowledge of the molecular mechanisms and potential targets causing childhood asthma is of utmost significance. Childhood asthma datasets were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) between asthmatic child and healthy people were screened by the Limma package. DEGs were subjected to further analyses utilizing GO, KEGG and GSEA analysis. The hub genes associated with childhood asthma were discovered by PPI analysis. The drugs target hub genes were accessed from the DrugBank database. Autodock vina was used to explore the binding ability of targeted drugs to hub genes. Total 80 DEGs were selected from GSE152004 and GSE65204 datasets. The cytokine-cytokine receptor interaction was the key pathway identified by functional enrichment analysis of shared DEGs. A total of 4 hub genes (CCL26, CXCR6, IL18RAP and CCL20) were identified by the constructed PPI network, among which CXCR6, IL18RAP and CCL20 were significantly decreased in childhood asthma datasets. Whereas, the CCL26 was significantly increased in childhood asthma datasets. Additionally, the extra dataset GSE19187 and GSE240567 were employed for validation. Ultimately, drugs (Cimetidine, Cefaclor and Propofol) that target hub genes have favorable combination ability. We have determined that CCL26, CXCR6, IL18RAP and CCL20 might have crucial involvement in the advancement of childhood asthma, thus having the potential to be targeted therapeutically in order to enhance treatment choices for childhood asthma. Statement of Integration, Innovation and Insight: The cytokine-cytokine receptor interaction is a key pathway in the occurrence of childhood asthma. The hub genes (CCL26, CXCR6, IL18RAP and CCL20) affect the development of childhood asthma. The drugs (Cimetidine, Cefaclor and Propofol) that target hub genes have favorable combination ability.