Metabolomic profiling of human bronchial/tracheal epithelial cells (hBTECs) after H1N1 infection
In previous studies, we have shown the critical role played by lipogenesis pathways in the life cycles of viruses. Building on this line of investigation, we sought to investigate the relevance of this pathway in the context of influenza A H1N1 virus (pdm09) infection, using human bronchial and tracheal epithelial cells (hBTECs) as our model system. To this end, we conducted targeted quantitation of polar metabolites in these cells. Our findings revealed that host glucose metabolism is a commonly affected pathway in response to viral infection. These results provide further evidence of the significance of metabolic pathways in the host-virus interaction and offer new insights into the molecular mechanisms underlying viral pathogenesis. To prepare for virus infection, 1E7 human brain microvascular endothelial cells (hBTECs) were seeded in a 10cm dish one day prior to the experiment. On day 1, the cells were infected with H1N1 virus at a multiplicity of infection (MOI) of either 0 or 5. After 24 hours, cell lysates were harvested and subjected to targeted metabolomics analysis using LC-MS/MS. Each treatment was repeated three times (n=3). A heatmap and log2-fold change (Log2FC) of metabolites were generated to compare the infection and non-infection groups. Metabolite set enrichment analysis was performed to identify the top 25 enriched pathways upon H1N1 infection. The analysis was conducted using the powerful MetaboAnalyst 5.0 software. The results were normalized based on cell number. Unpaired Student's t-test was employed to perform statistical analysis of the data. This study provides valuable insights into the metabolic response of hBTECs to H1N1 infection and sheds light on potential therapeutic targets for this viral infection.