Integration of transcriptomics, proteomics and metabolomics data to reveal the biological mechanisms of abrin injury in human lung epithelial cells.

• We performed multi-omics studies to reveal abrin lung injury mechanism. • A set of genes, proteins and metabolite were identified as the biomarker. • Provided large-scale omics data for abrin poisoning. Abrin toxin (AT) is a potent plant toxin that belongs to the type Ⅱ ribosome inactivating protein family and is recognized as an important toxin agent for potential bioweapons. Exposure to AT by way of aerosol is the most lethal route, but the mechanism of injury requires further investigation. In the present study, we performed a comprehensive analysis of transcriptomics, proteomics and metabolomics on the potential mechanism of abrin injury in human lung epithelial cells. In total, 6838 genes, 314 proteins and 178 metabolites showed significant changes in human lung epithelial cells after AT treatment. Using molecular function, pathway, and network analysis, the genes and proteins regulated in AT-treated cells were mainly attributed to amino acid metabolism, lipid metabolism, and genetic information processing. Furthermore, a comprehensive analysis of the transcripts, proteins, and metabolites was performed. The results revealed that the correlated genes, proteins, and metabolism pathways regulated in AT-treated human lung epithelial cells were involved in tryptophan metabolism, biosynthesis of amino acids, and protein digestion and absorption. This study provides large-scale omics data to develop new strategies for the prevention, rapid diagnosis, and treatment of AT poisoning, especially AT from aerosol. [ABSTRACT FROM AUTHOR]