Identification microenvironment immune features and key genes in elderly stroke patients

Abstract

Background: The purpose of this study was to identify the signaling pathways and immune microenvironments related to elderly stroke patients.

Methods: We downloaded the public transcriptome data (GSE37587) from the gene expression omnibus and divided the patients into young and old groups and identified differentially expressed genes (DEGs). Gene ontology function analysis, Kyoto encyclopedia of genes and genomes pathway analysis, and gene set enrichment analysis (GSEA) were performed. A protein-protein interaction network was constructed and hub genes were identified. Gene-miRNA, gene-TF, and gene-drug networks were constructed using the network analyst database. The immune infiltration score was evaluated using single-sample gene set enrichment analysis GSEA, its correlation with age was computed and visualized using R software.

Results: We identified 240 DEGs, including 222 upregulated and 18 downregulated DEGs. Gene ontology enrichment was significantly enriched in response to the virus, type I interferon signaling pathway, cytological component, focal adhesion, cell-substrate adherents junction, and the cytosolic ribosome. GSEA identified the following mechanisms: heme metabolism, interferon gamma response, and interferon alpha response. Ten hub genes included interferon alpha-inducible protein 27, human leucocyte antigen-G, interferon-induced protein with tetratricopeptide repeats 2, 2'-5'-oligoadenylate synthetase 2, interferon alpha-inducible protein 6, interferon alpha-inducible protein 44-like, interferon-induced protein with tetratricopeptide repeats 3, interferon regulatory factor 5, myxovirus resistant 1, and interferon-induced protein with tetratricopeptide repeats 1. Quantitative analysis of immune infiltration showed that increased age was significantly positively correlated with myeloid-derived suppressor cells and natural killer T cells, and negatively correlated with immature dendritic cells.

Conclusion: The present research could help us better understand the molecular mechanisms and immune microenvironment of elderly patients with stroke.