Pathway analysis of sepsis-induced changes gene expression

Abstract

Abstract Background Sepsis reaction is a response to an infection composed of genetic elements. This research aims to better understand how sepsis affects the molecular pathways in whole blood samples. Methods Whole blood samples from healthy controls (n = 18), sepsis nonsurvivors (n = 9), and sepsis survivors (n = 26) were retrieved from the gene expression omnibus (GEO) collection of the national center for biotechnology information (NCBI) (accession number GSE54514). The NCBI's GEO2R program was used to determine differential expression, and the ingenuity pathway analysis (IPA) software was utilized to do a pathway analysis. Results In sepsis patients, 2672 genes were substantially differently expressed (p value 0.05). One thousand three hundred four genes were overexpressed, and one thousand three hundred sixty-eight were under-expressed. The inhibition of ARE-mediated mRNA degradation pathway and the Pl3K/AKT signaling spliceosomal cycle were the most significant canonical pathways identified by ingenuity pathway analysis (IPA). The IPA upstream analysis predicted the ESR1, SIRT1, and PTPRR proteins, and the drugs filgrastim and fluticasone were top transcriptional regulators. Conclusions The inhibition of ARE-mediated mRNA degradation pathway and the Pl3K/AKT signaling spliceosomal cycle were highlighted as essential pathways of inflammation by IPA, indicating widespread cancer owing to sepsis. Our data imply that sepsis considerably influences gene pathways in whole blood samples, pointing to possible targets for sepsis treatment.