Figure 4
Figure 4. Acute local administration of G-CSF promotes Mac-1–dependent adhesion and transendothelial migration of neutrophils in vivo. (A) Leukocyte rolling flux and (B) adhesion in postcapillary venules (vessel diameter 25-40 μm) of cremaster muscle before and after superfusion with saline or 15 μg/mL G-CSF for up to 30 minutes in WT C57BL/6 mice. n = 6 to 8 mice per group. *P < .05; **P < .001 versus basal adhesion, or versus saline rolling flux. (C) In vivo confocal image using PE-conjugated anti–Gr-1 mAb showing that adherent cells in G-CSF–treated muscle are Gr-1+ neutrophils. (D) Leukocyte rolling flux, (E) adhesion, and (F) transendothelial migration in postcapillary venules of cremaster muscle before and after superfusion with 15 μg/mL G-CSF for up to 45 minutes in WT C57BL/6 mice that were pretreated (intravenous injection) with anti–Mac-1 mAb (5C6) or isotype control mAb. n = 5 mice per group. Data represent mean plus or minus SEM; *P < .05; **P < .001.

Acute local administration of G-CSF promotes Mac-1–dependent adhesion and transendothelial migration of neutrophils in vivo. (A) Leukocyte rolling flux and (B) adhesion in postcapillary venules (vessel diameter 25-40 μm) of cremaster muscle before and after superfusion with saline or 15 μg/mL G-CSF for up to 30 minutes in WT C57BL/6 mice. n = 6 to 8 mice per group. *P < .05; **P < .001 versus basal adhesion, or versus saline rolling flux. (C) In vivo confocal image using PE-conjugated anti–Gr-1 mAb showing that adherent cells in G-CSF–treated muscle are Gr-1+ neutrophils. (D) Leukocyte rolling flux, (E) adhesion, and (F) transendothelial migration in postcapillary venules of cremaster muscle before and after superfusion with 15 μg/mL G-CSF for up to 45 minutes in WT C57BL/6 mice that were pretreated (intravenous injection) with anti–Mac-1 mAb (5C6) or isotype control mAb. n = 5 mice per group. Data represent mean plus or minus SEM; *P < .05; **P < .001.

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