Figure 3
Figure 3. TLR2- or MyD88-deficient mice exhibit diminished granulocyte differentiation in S aureus–infected wounds. Wounds from WT mice, TLR2-deficient, and MyD88-deficient mice were collected 3 days after wounding (+/− S aureus inoculation). (A) Total lineage-negative/c-kit+ HSPCs isolated from wounds of WT mice and TLR2- or MyD88-deficient mice as evaluated by flow cytometry. (B) Lineage−/Sca-1+/c-kit+ cells (LSKs), CMPs, promyelocytes, and PMN/band neutrophils were enumerated from infected wounds by flow cytometry. (C) Wounds were collected on day 3 after wounding, and lineage-negative HSPCs were enriched from wound digest using magnetic beads. HSPCs were plated at equal density from all conditions. Ex vivo production of granulocyte-containing colonies from infected vs saline control wounds were counted. Panels A and B represent 5 to 8 mice per group during 2 experiments, and panel C represents 4 mice per group. All data expressed as mean ± SEM for each condition (*P < .05; **P < .01; ***P < .001).

TLR2- or MyD88-deficient mice exhibit diminished granulocyte differentiation in S aureusinfected wounds. Wounds from WT mice, TLR2-deficient, and MyD88-deficient mice were collected 3 days after wounding (+/−S aureus inoculation). (A) Total lineage-negative/c-kit+ HSPCs isolated from wounds of WT mice and TLR2- or MyD88-deficient mice as evaluated by flow cytometry. (B) Lineage/Sca-1+/c-kit+ cells (LSKs), CMPs, promyelocytes, and PMN/band neutrophils were enumerated from infected wounds by flow cytometry. (C) Wounds were collected on day 3 after wounding, and lineage-negative HSPCs were enriched from wound digest using magnetic beads. HSPCs were plated at equal density from all conditions. Ex vivo production of granulocyte-containing colonies from infected vs saline control wounds were counted. Panels A and B represent 5 to 8 mice per group during 2 experiments, and panel C represents 4 mice per group. All data expressed as mean ± SEM for each condition (*P < .05; **P < .01; ***P < .001).

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