Bioinformatic Analysis of Neuroimmune Mechanism of Neuropathic Pain

Abstract EN

Background.

Neuropathic pain (NP) is a devastating complication following nerve injury, and it can be alleviated by regulating neuroimmune direction.

We aimed to explore the neuroimmune mechanism and identify some new diagnostic or therapeutic targets for NP treatment via bioinformatic analysis.

Methods.

The microarray GSE18803 was downloaded and analyzed using R.

The Venn diagram was drawn to find neuroimmune-related differentially expressed genes (DEGs) in neuropathic pain.

Gene Ontology (GO), pathway enrichment, and protein-protein interaction (PPI) network were used to analyze DEGs, respectively.

Besides, the identified hub genes were submitted to the DGIdb database to find relevant therapeutic drugs.

Results.

A total of 91 neuroimmune-related DEGs were identified.

The results of GO and pathway enrichment analyses were closely related to immune and inflammatory responses.

PPI analysis showed two important modules and 8 hub genes: PTPRC, CD68, CTSS, RAC2, LAPTM5, FCGR3A, CD53, and HCK.

The drug-hub gene interaction network was constructed by Cytoscape, and it included 24 candidate drugs and 3 hub genes.

Conclusion.

The present study helps us better understand the neuroimmune mechanism of neuropathic pain and provides some novel insights on NP treatment, such as modulation of microglia polarization and targeting bone resorption.

Besides, CD68, CTSS, LAPTM5, FCGR3A, and CD53 may be used as early diagnostic biomarkers and the gene HCK can be a therapeutic target.