Fig. 9.
GM-CSF inhibits apoptosis (A), reverses downregulation of superoxide release (B), and suppresses caspase activation (C and D) in TNF-–treated neutrophils. Neutrophils were pretreated with 1, 10, and 100 ng/mL GM-CSF for 1 hour before the addition of TNF- plus cycloheximide. DNA fragmentation (A), superoxide release in response to PMA (B), and the presence of DEVD-cleaving (C) or zEK(bio)D-aomk-binding (D) active caspases were analyzed after incubation for the indicated time period (B) or for 2 hours (A, C, and D). (E) Cells were pretreated with 100 μmol/L zVAD-fmk or 10 ng/mL GM-CSF singly and in combination before addition of TNF-/cycloheximide for 2 hours followed by measurement of PMA-induced superoxide release. Values represent the means + SEM of three independent experiments performed in duplicate.

GM-CSF inhibits apoptosis (A), reverses downregulation of superoxide release (B), and suppresses caspase activation (C and D) in TNF-–treated neutrophils. Neutrophils were pretreated with 1, 10, and 100 ng/mL GM-CSF for 1 hour before the addition of TNF- plus cycloheximide. DNA fragmentation (A), superoxide release in response to PMA (B), and the presence of DEVD-cleaving (C) or zEK(bio)D-aomk-binding (D) active caspases were analyzed after incubation for the indicated time period (B) or for 2 hours (A, C, and D). (E) Cells were pretreated with 100 μmol/L zVAD-fmk or 10 ng/mL GM-CSF singly and in combination before addition of TNF-/cycloheximide for 2 hours followed by measurement of PMA-induced superoxide release. Values represent the means + SEM of three independent experiments performed in duplicate.

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