Fig. 6: Severe influenza infection induces transcriptional shutdown and activation of ECM reorganization and antiviral immune pathways.
From: An immune-competent lung-on-a-chip for modelling the human severe influenza infection response
a, The number of highly upregulated genes (FC >1.5) per cell type compared with the control devices. b, Volcano plot visualization of DEG analysis, highlighting all genes significantly highly (P < 0.05, |FC| >1.5) up- or downregulated across all cell populations when comparing uninfected control to 8 h H1N1 infection IC-LOC devices. Statistical significance determined via Wilcoxon rank sum test. c,d, Pathways represented in the top 10% of upregulated genes in each infected condition, comprised primarily of immune pathways (c) and ECM interactions (d). Statistical significance determined via binomial test. e, Heat map of expression levels of inflammatory, antiviral and immune activation genes in B, CD4 T, CD8 T and NK/NKT cells from uninfected and infected devices showing increased expression levels in the infected devices. Heat map shows average expression levels of each gene for cells with non-zero expression. White boxes represent genes that are not expressed in the given cell type. f, Heat map of expression levels of innate immune response genes in AM, DC, IM, endothelial, fibroblast, adventitial and myofibroblast populations. g, Top 10% of CellChat predicted cell–cell interactions, demonstrating an increase in both stromal and immune cell interactions in response to infection. DEGs, differentially expressed genes; Mon, monocytes; Gran, granulocytes; Adv, adventitial cells; Fib, fibroblasts; Myofib, myofibroblasts; Endo, endothelial cells; Epi, epithelial cells; TFs, transcription factors; pval, P value.
