Identification of genes and pathways associated with multiple organ dysfunction syndrome by microarray analysis

Multiple organ dysfunction syndrome (MODS) is characterized by the development of progressive physiological dysfunction of ≥2 organs or organ systems and is responsible for the majority of the morbidity and mortality among patients in intensive care units. The aim of the present study was to investigate the potential genes and pathways associated with MODS. The microarray dataset GSE60088 was downloaded from the Gene Expression Omnibus and used to identify differentially expressed genes (DEGs) between organ tissues (lung, liver and kidney) obtained from a murine model of MODS and healthy controls. The interactions between DEGs in lungs, liver and kidneys were revealed by Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. Furthermore, protein‑protein interaction (PPI) data for DEGs were obtained from the Search Tool for the Retrieval of Interacting Genes and a PPI network was constructed. Additionally, DEGs that were common among the three organs were screened and transcription factors that regulated them were predicted using the iRegulon plugin. A total of 943, 267 and 227 DEGs were identified in lung, liver and kidney samples, respectively, between mice with MODS and healthy controls. In lung and liver samples, two pathways that were enriched with DEGs were identified and were common between lung and liver samples, including 'cytokine‑cytokine receptor interaction' and 'Jnk‑STAT signaling pathway', and examples of DEGs associated with these pathways include C‑X‑C motif chemokine ligand (Cxcl)1 and Cxcl10, and signal transducer and activator of transcription (Stat)1, respectively. Furthermore, two common pathways were identified in liver and kidney samples, which included 'MAPK signaling pathway' and 'p53 signaling pathway', and DEGs associated with these pathways included growth arrest and DNA damage‑inducible α. A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.