Figure 1
Dasatinib abrogates adhesion-dependent respiratory burst of human neutrophils. Human neutrophils pretreated with the indicated concentrations of dasatinib were stimulated with 20 ng/mL of human TNF, 50 ng/mL of human C5a, 1 μg/mL of Pam3CSK4 or 1 μg/mL of ultrapurified LPS (upLPS) while adherent to a fibrinogen (Fbg)–coated (A,F) or FCS-coated (B,E) surface; by plate-bound Abs against human CD18 (C), by plating them on a poly-RGD–coated surface (D); or by 100nM PMA (E); followed by spectrophotometric measurement of superoxide release (A-E) or luminometric measurement of reactive oxygen production (F). Kinetic curves show mean and SD of representative experiments and dose-response curves show mean and SEM of the percent response from 3-11 independent experiments. RLU indicates relative luminescence unit.

Dasatinib abrogates adhesion-dependent respiratory burst of human neutrophils. Human neutrophils pretreated with the indicated concentrations of dasatinib were stimulated with 20 ng/mL of human TNF, 50 ng/mL of human C5a, 1 μg/mL of Pam3CSK4 or 1 μg/mL of ultrapurified LPS (upLPS) while adherent to a fibrinogen (Fbg)–coated (A,F) or FCS-coated (B,E) surface; by plate-bound Abs against human CD18 (C), by plating them on a poly-RGD–coated surface (D); or by 100nM PMA (E); followed by spectrophotometric measurement of superoxide release (A-E) or luminometric measurement of reactive oxygen production (F). Kinetic curves show mean and SD of representative experiments and dose-response curves show mean and SEM of the percent response from 3-11 independent experiments. RLU indicates relative luminescence unit.

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