Data driven analysis reveals prognostic genes and immunological targets in human sepsis associated acute kidney injury

BACKGROUND:The molecular mechanism of sepsis-associated acute kidney injury (SA-AKI) is unclear.We analyzed co-differentially expressed genes (co-DEGs) to elucidate the underlying mechanism and intervention targets of SA-AKI. METHODS:The microarray datasets GSE65682, GSE30718, and GSE174220 were downloaded from the Gene Expression Omnibus (GEO) database.We identified the co-DEGs and constructed a gene co-expression network to screen the hub genes.We analyzed immune correlations and disease correlations and performed functional annotation of the hub genes.We also performed single-cell and microenvironment analyses and investigated the enrichment pathways and the main transcription factors.Finally, we conducted a correlation analysis to evaluate the role of the hub genes.RESULTS: Interleukin 32 (IL32) was identified as the hub gene in SA-AKI, and the main enriched signaling pathways were associated with hemopoiesis, cellular response to cytokine stimulus, inflammatory response, and regulation of kidney development.Additionally, IL32 was significantly associated with mortality in SA-AKI patients.Monocytes, macrophages, T cells, and NK cells were closely related to IL32 and were involved in the immune microenvironment in SA-AKI patients.IL32 expression increased significantly in the kidney of septic mouse.Toll-like receptor 2 (TLR2) was significantly and negatively correlated with IL32.CONCLUSION: IL32 is the key gene involved in SA-AKI and is significantly associated with prognosis.TLR2 and relevant immune cells are closely related to key genes.