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Wound monocyte-derived macrophage plasticity controls the initiation and resolution of inflammation that is critical for proper healing, however, in diabetes mellitus, the resolution of inflammation fails to occur. In diabetic wounds, the kinetics of blood monocyte recruitment and the mechanisms that control in vivo monocyte/macrophage differentiation remain unknown.

Here, we characterized the kinetics and function of Ly6C^Hi [Lin⁻ (CD3⁻CD19⁻NK1.1⁻Ter-119⁻) Ly6G⁻CD11b⁺] and Ly6C^Lo [Lin⁻ (CD3⁻CD19⁻NK1.1⁻Ter-119⁻) Ly6G⁻CD11b⁺] monocyte/macrophage subsets in normal and diabetic wounds. Using flow-sorted tdTomato-labeled Ly6C^Hi monocyte/macrophages, we show Ly6C^Hi cells transition to a Ly6C^Lo phenotype in normal wounds, whereas in diabetic wounds, there is a late, second influx of Ly6C^Hi cells that fail transition to Ly6C^Lo. The second wave of Ly6C^Hi …