scRNA-seq of AML-exposed neutrophils reveals altered granulopoiesis, decreased maturation score, and increased inflammation scores. (A) Bidimensional UMAP analysis of 4438 BM neutrophils from control mice separated into 3 clusters NEU1, NEU2, and NEU3. (B) Heat map of DEGs from each cluster. (C) Bidimensional UMAP analysis of healthy BM neutrophils (blue) and AML-exposed neutrophils (red). (D) Frequency of each NEU cluster as a percentage of total cells. (E) Maturation score of each NEU cluster. (F) Inflammation score of each NEU cluster. (G) Expression of C/EBPβ transcripts in each NEU cluster. (H) Volcano plot displaying DEG of NEU2 AML-exposed neutrophils (red; 205 genes) vs NEU2 healthy neutrophils (blue; 322 genes). (I) Gene ontology analysis of DEGs in panel H. All DEGs have fold change >1.5; P ≤ .05. Significance is denoted as ∗∗∗∗P ≤ .0001; ∗∗∗P ≤ .001; ∗P ≤ .05; ns P > .05 (using 1-way ANOVA in panels E-G).
Figure 3.

scRNA-seq of AML-exposed neutrophils reveals altered granulopoiesis, decreased maturation score, and increased inflammation scores. (A) Bidimensional UMAP analysis of 4438 BM neutrophils from control mice separated into 3 clusters NEU1, NEU2, and NEU3. (B) Heat map of DEGs from each cluster. (C) Bidimensional UMAP analysis of healthy BM neutrophils (blue) and AML-exposed neutrophils (red). (D) Frequency of each NEU cluster as a percentage of total cells. (E) Maturation score of each NEU cluster. (F) Inflammation score of each NEU cluster. (G) Expression of C/EBPβ transcripts in each NEU cluster. (H) Volcano plot displaying DEG of NEU2 AML-exposed neutrophils (red; 205 genes) vs NEU2 healthy neutrophils (blue; 322 genes). (I) Gene ontology analysis of DEGs in panel H. All DEGs have fold change >1.5; P ≤ .05. Significance is denoted as ∗∗∗∗P ≤ .0001; ∗∗∗P ≤ .001; ∗P ≤ .05; ns P > .05 (using 1-way ANOVA in panels E-G).

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