Exploring a shared genetic signature and immune infiltration between spontaneous intracerebral hemorrhage and Helicobacter pylori infection.

Background: Spontaneous intracerebral hemorrhage (ICH) is a devastating form of stroke with high morbidity, disability and mortality. Helicobacter pylori is a major pathogen responsible for chronic gastritis, leading to gastric ulcers and ultimately gastric cancer. Although it remains controversial whether H. pylori infection causes peptic ulcers under various traumatic stimuli, some related studies suggest that H. pylori infection may be an important factor in delaying peptic ulcer healing. However, the linking mechanism between ICH and H. pylori infection remain unclear. The purpose of this study was to examine the genetic features and pathways shared in ICH and H. pylori infection, and compare immune infiltration.

Methods: We used microarray data for ICH and H. pylori infection from the Gene Expression Omnibus (GEO) database. Differential gene expression analysis was performed on both datasets using the R software and the limma package to find the common differentially expressed genes (DEGs). In addition, we performed functional enrichment analysis on DEGs, determined protein-protein interactions (PPIs), identified Hub genes using the STRING database and Cytoscape software, and constructed microRNA-messenger RNA (miRNA-mRNA) interaction networks. Additionally, immune infiltration analysis was performed with the R software and related R packages.

Results: A total of 72 DEGs were identified between ICH and H. pylori infection, including 68 upregulated genes and 4 downregulated genes. Functional enrichment analysis revealed that multiple signaling pathways are closely linked to both diseases. In addition, the cytoHubba plugin identified 15 important hub genes, namely PLEK, NCF2, CXCR4, CXCL1, FGR, CXCL12, CXCL2, CD69, NOD2, RGS1, SLA, LCP1, HMOX1, EDN1, and ITGB3.Also, the correlation analysis of immune cell fractions revealed a limited link between their immune-related common genes and immune cells.

Conclusion: Through bioinformatics methods, this study revealed that there are common pathways and hub genes between ICH and H. pylori infection. Thus, H. pylori infection may have common pathogenic mechanisms with the development of peptic ulcer after ICH. This study provided new ideas for early diagnosis and prevention of ICH and H. pylori infection.