[Ca2+]i-transients and actin polymerization in human neutrophils under stimulation with GROα and complement fragment C5a

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Abstract
The neutrophil chemotaxins, complement fragment C5a (C5a) and GROα, induced the mobilization of Ca2+ from intracellular stores and the polymerization of actin in human neutrophils as assayed by flow cytometric measurements. [Ca2+]i-transients developed as an “all-or-none” response. Individual neutrophils required different threshold concentrations of added ligand to induce [Ca2+]i-transients which were then always maximal. In contrast, chemotaxin-induced formation of actin filaments in single neutrophils occurred in a dose-dependent manner. Pertussis toxin blocked chemotaxin-induced actin polymerization and [Ca2+]i-transients indicating that both cell responses shared initial activation steps such as ligand binding and activation of guanine nucleotide-binding proteins (G-proteins).