TLR2/MyD88 signaling is required in HSPCs but not in the wound environment for granulopoiesis in S aureus–infected wounds. In panels A and B, infected wounds were injected with HSPCs from transgenic WT or MyD88-deficient Lys-EGFP mice. Fluorescent signal from EGFP-PMNs in the wound was recorded 7 days after injection as a read-out for HSPC differentiation to PMNs. Fluorescence was measured as the total flux of EGFP in photons per centimeters squared per second. (A) BM HSPCs from WT Lys-EGFP mice were directly injected as depicted into S aureus–infected wounds of WT mice and TLR2- or MyD88-deficient mice. EGFP-PMN fluorescence in the wound is shown. (B) BM HSPCs from WT Lys-EGFP mice or MyD88^−/−/Lys-EGFP mice were injected into S aureus–infected wounds of WT mice. EGFP-PMN fluorescence in the wound is shown. (C) TLR2-deficient Lys-EGFP mice were not available, so BM HSPCs were harvested from WT or TLR2-deficient mice (CD45.2) and were injected into the S aureus–inoculated wounds of CD45.1 congenic mice. Skin wounds were collected at day 7 after transfer, and the number of donor-derived CD45.2⁺ PMNs per milligrams of wound tissue was analyzed via flow cytometry. The number of HSPC-produced PMNs is shown as the number of donor-derived CD45.2⁺ PMNs per milligrams of wound tissue. Data represent 3 mice per group and are displayed as mean ± SEM (**P < .01; ***P < .001).