抄録
The mechanism of chemotactic peptide-induced priming of the respiratory burst was explored, by using human granulocytes and peripheral blood granulocytes from the colony-stimulating factor producing tumor-bearing nude mice. N-formyl-methionyl-leucyl-phenylalanine (fMet-Leu-phe) induced the transient increase in cytoplasmic free Ca2+, [Ca2+] i, whereas fMet-Leu-Phe induced neither superoxide (O-2) release nor membrane potential changes (depolarizaion) in mouse granulocytes. On the other hand, phorbol myristate acetate (PMA) induced O-2 release and membrane depolarization without inducing an increase in [Ca2+] i. The pretreatment of cells with fMet-Leu-Phe for 5 min at 37°C enhanced O-2 release and membrane depolarization stimulated by PMA (1-100 ng/ml) . The dose response curves for triggering of an increase in [Ca2+] i by fMet-Leu-Phe were identical to those for priming the cells. Similar results were obtained in human granulocytes.
Furthermore, the pretreatment of cells with Ca2+ ionophore ionomycin enhanced O-2 release and membrane depolarization stimulated by PMA. These findings suggest that an increase in [Ca2+] i by itself is not sufficient to trigger the respiratory burst and membrane potential changes, and that fMet-Leu-Phe-induced priming is caused by an increase in [Ca2+] i.
