rhAPC inhibits neutrophil adhesion and migration. (A) Binding of 10 nM fMLP-treated neutrophils to immobilized FN in the presence of various concentrations of rhAPC. For each condition, binding was measured in triplicate and stated as mean (± SEM). *P < .05 versus fMLP-treated cells in the absence of rhAPC. (B) Migration of human neutrophils on FN-coated cover glasses in the presence of fMLP ± rhAPC. Cells were tracked over a 30-minute period, and each line represents one cell. Experiments were repeated on neutrophil preparations from 3 independent donors. (C) Directional migration of neutrophils, as measured by the underagarose migration assay. The number of control or rhAPC-treated neutrophils migrating to fMLP (1 and 2) or to PBS (3) was counted. Results are expressed as mean ± SEM of 3 experiments from 2 independent donors. (D) Center-zeroed tracks of control or rhAPC-treated neutrophils migrating toward microtips containing fMLP. The scale of each graph is in microns. The speed (S, μm s⁻¹), migratory index (MI), and X^D (mean direction in which the population is moving, in degrees) are shown (mean ± SEM). (E) Migration of human neutrophils on FN-coated cover glasses in the presence of IL-8 ± rhAPC. (F) Cytosolic Ca²⁺ levels in stirred Fluo-4–labeled neutrophils were continuously measured in a fluorometer. Control (PBS) or rhAPC-treated neutrophils in Ca²⁺-containing buffer were sequentially stimulated with 10 nM fMLP and 40 μM digitonin. The data are representative of at least 3 independent experiments.