Integrin α9 and VCAM-1 interactions promote gene expressions related to neutrophil inflammation, exocytosis, NF-κB signaling, and chemotaxis. (A) Schematic of experimental design. (B) Principal component analysis was performed based on RNA-seq of stimulated and unstimulated WT neutrophils and (C) stimulated neutrophils from littermate controls and neutrophil–specific integrin α9^−/− mice. (D) Volcano plots of differentially expressed genes (DEGs) based on RNA-seq analysis of stimulated and unstimulated WT neutrophils and (E) stimulated neutrophils from littermate controls and neutrophil–specific integrin α9^−/− mice. (F) Log fold-change of all the shared DEGs from stimulated and unstimulated WT neutrophils and stimulated neutrophils from littermate controls and neutrophil–specific integrin α9^−/− mice. (G) Log fold-change of selected genes from DEGs of stimulated and unstimulated WT neutrophils. (H) Log fold-change of selected genes from DEGs of neutrophils from littermate controls and neutrophil–specific integrin α9^−/− mice. (I) GSEA was performed based on RNA-seq of stimulated and unstimulated WT neutrophils and (J) stimulated neutrophils from littermate controls and neutrophil–specific integrin α9^−/− mice. The significance of the enriched pathways was determined by right-tailed Fisher exact test followed by Benjamini-Hochberg multiple testing adjustment; n = 5 (B,D,G,I); and n = 4-5 (C,E,F,H,J). GSEA, gene set enrichment analysis.