Fig. 3. Airway macrophages are transcriptionally primed to support epithelial repair and display IL-33-ST2 activation during their differentiation process.

a–e Transcriptional profiling of myeloid cell subsets flow-sorted from naïve and NA-treated mice on d6. a Principal component analysis (PCA) of the transcriptomes of flow-sorted monocytes (P1), monocyte-derived macrophages (P2), and resident AAMs (P3) performed on all expressed genes identified from a generalized linear model to perform an ANOVA-like test for differential expression between any conditions in the dataset (FDR step-up procedure q-value < 0.05. b k-means clustering of all identified genes revealed core gene signatures specific to P1 (Cluster I), P2 (Cluster II), and P3 (Cluster III). The pathway enriched processes associated with each cluster are shown on the bottom of the heatmap. Scale bar on the bottom denotes relative log₂ differences in gene expression for each row. c Heatmaps showing the top relative expression of DEG that are associated with macrophage ability to modulate the epithelial cell niche. Those functions include growth factors secretion, extracellular matrix (ECM) remodeling and immune response regulation between P2 and P3 cells. d, e Score plot illustrating the signal transduction pathways upregulated in Cluster I (d), highlighting the overrepresentation of IL-33 signaling and MyB88/NFkb axis in the different subsets of myeloid cells (e).