HIF‑1 and macrophage activation signalling pathways are potential biomarkers of invasive aspergillosis.

Invasive aspergillosis (IA) is a severe disease, the pathogenesis of which remains unclear. The present study aimed to determine the molecular mechanism of IA and to identify potential biomarkers using bioinformatics analysis. The GSE78000 dataset, which includes data from patients with IA and healthy individuals, was downloaded from Gene Expression Omnibus. Differentially expressed genes (DEGs) between the IA and control groups were identified with the 'affy' package in R software. The Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) databases were then used to analyse the function and pathway enrichment of DEGs. The protein-protein interaction network was analysed with the Search Tool for the Retrieval of Interacting Genes (STRING) website. In addition, DEGs were confirmed using reverse transcription-quantitative PCR and western blotting in samples with IA (n=6) and control samples (n=6) collected from the Department of Respiratory and Critical Care Medicine of the First Affiliated Hospital of Henan University of Science and Technology (Luoyang, China). The present study identified 735 DEGs, including 312 upregulated and 423 downregulated genes. Through GO and KEGG analyses of the DEGs, macrophage activation and hypoxia-inducible factor 1 (HIF-1) signalling pathways were revealed to be significantly upregulated and downregulated, respectively, in patients with IA compared with that of the healthy individuals. Subsequently, correlation analysis of macrophage activation and HIF-1 signalling pathways was revealed using correlation as a distance metric for hierarchical clustering correlation analysis. However, there was no protein-protein interaction between the macrophage activity regulation and HIF-1 signalling pathways based on STRING analysis. In summary, the present study identified candidate genes and associated molecules that may be associated to IA and revealed potential biomarkers and therapeutic targets for IA.