Botulinum C2 toxin was employed as a specific inhibitor of actin polymerization in rat neutrophils to determine its role in oxidase activation. This toxin was shown to inhibit actin polymerization and the microfilament-dependent function, phagocytosis. Oxidase activation in response to the chemotactic peptide, f-Met-Leu-Phe (FMLP) was enhanced approx. 3-fold. The enhancement by C2 toxin did not occur in cells pretreated with cytochalasin B. C2 toxin had no significant effect on the FMLP-induced intracellular Ca2+ rise. These data are consistent with an inhibitory role for actin polymerization in oxidase activation.
