Figure 5.
Figure 5. STAT3-deficient mice have impaired acute neutrophil mobilization in response to G-CSF. (A) Peripheral blood samples were analyzed by flow cytometry following red blood cell lysis to determine the percentage of Gr-1+/CD11b+ cells present in untreated mice or mice that received G-CSF (250 μg/kg) 24 hours prior to analysis. The amount of Gr-1+/CD11b+ cells in G-CSF–treated samples was normalized to the amount in untreated controls of the appropriate genotype to provide the relative level of Gr-1+/CD11b+ cells in the blood following G-CSF treatment. Relative Gr-1+/CD11b+ levels for wild-type (WT, □) and STAT3-deficient (KO, ▪) mice are shown (n = 6 for WT, n = 5 for KO) (P = .003 comparing WT with KO). (B) Blood samples were subjected to automated counting to determine total neutrophil numbers in untreated mice or mice that received G-CSF (250 μg/kg) 24 hours prior to analysis. Neutrophil amounts in G-CSF–treated samples were normalized to amounts in untreated controls of the appropriate genotype to determine the relative induction by G-CSF. Relative neutrophil levels for WT (□) and KO (▪) are shown (n = 6 for WT, n = 5 for KO) (P = .002 comparing WT with KO). Error bars represent SEM in both panels.

STAT3-deficient mice have impaired acute neutrophil mobilization in response to G-CSF. (A) Peripheral blood samples were analyzed by flow cytometry following red blood cell lysis to determine the percentage of Gr-1+/CD11b+ cells present in untreated mice or mice that received G-CSF (250 μg/kg) 24 hours prior to analysis. The amount of Gr-1+/CD11b+ cells in G-CSF–treated samples was normalized to the amount in untreated controls of the appropriate genotype to provide the relative level of Gr-1+/CD11b+ cells in the blood following G-CSF treatment. Relative Gr-1+/CD11b+ levels for wild-type (WT, □) and STAT3-deficient (KO, ▪) mice are shown (n = 6 for WT, n = 5 for KO) (P = .003 comparing WT with KO). (B) Blood samples were subjected to automated counting to determine total neutrophil numbers in untreated mice or mice that received G-CSF (250 μg/kg) 24 hours prior to analysis. Neutrophil amounts in G-CSF–treated samples were normalized to amounts in untreated controls of the appropriate genotype to determine the relative induction by G-CSF. Relative neutrophil levels for WT (□) and KO (▪) are shown (n = 6 for WT, n = 5 for KO) (P = .002 comparing WT with KO). Error bars represent SEM in both panels.

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