Identification of hub genes and potential biomarkers of neutrophilic asthma: evidence from a bioinformatics analysis

Abstract

Objective

Asthma is a chronic airway inflammatory disease caused by multiple genetic and environmental factors. This study mainly sought to provide potential therapeutic targets and biomarkers for neutrophilic asthma (NA).

Methods

Three gene expression profiling datasets were obtained from the Genome Expression Omnibus (GEO) database. GSE45111 and GSE41863 were used to identify hub genes and potential biomarkers, and GSE137268 was used for data verification. We verified the repeatability of intragroup data and identified differentially expressed genes (DEGs). Then, we conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the DEGs, and a protein–protein interaction (PPI) network was constructed to identify the hub genes. Finally, receiver operating characteristic (ROC) analysis was used to verify the ability of the hub genes to differentiate between NA and eosinophilic asthma (EA).

Results

In this study, we identified 411 DEGs by comprehensive analysis of NA/EA patients and NA/healthy controls (HCs). Ten hub genes (CXCR1, FCGR3B, CXCR2, SELL, S100A12, CSF3R, IL6R, JAK3, CD48, and GNG2) were identified from the PPI network. Finally, based on the ROC analysis, 7 genes showed good diagnostic value for discriminating NA from EA—CXCR1, FCGR3B, CXCR2, SELL, S100A12, CSF3R, and IL6R (AUC > 0.7).

Conclusion

We identified 7 hub genes that can distinguish NA from EA. The IL-8-mediated signaling may be the primary pathway to determine the NA phenotype in asthma. CXCR1/2 and S100A12 may be the primary genes determining the NA phenotype. CXCR1/2 and S100A12 might be biomarkers and new therapeutic targets for NA.

Supplemental data for this article is available online at at

Keywords:

• Biomarkers
• hub gene
• neutrophilic asthma
• interleukin-8 mediated signaling
• S100A12
• CXCR1/2

Acknowledgements

Hanxiang Nie made substantial contributions to the conception and design of the study. Qibin Lin performed the research and wrote the article. Haiyang Ni, Jieying Zhong and Zhishui Zheng analysis the data.

Declaration of interest

The authors report no conflict of interest.

Data availability statement

Not applicable.

Additional information

Funding

This work was supported by grants from the National Natural Science Foundation of China (No. 82170021).