An oxidative metabolic burst comparable to that after phagocytosis was initiated in normal PMN by exposing them to sera incubated with powdered inulin. In these sera a change in the electrophoretic mobility of the C3PA from beta to gamma indicated activation of the alternate pathway, while consumption of C3 indicated C activation. An increase of hexose monophosphate shunt activity in PMN greater than 5-fold indicated stimulation. Increases in O2 consumption, NBT dye reduction, and degranulation

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... confirmed the metabolic burst. PMN metabolism was stimulated by inulin in fresh sera and in sera depleted of C4 from patients with active hereditary angioneurotic edema. Stimulation did not occur in the absence of serum, in sera heated to 50°C or 56°C for 30 min, in 0.02 M EDTA serum, in sera depleted of C3 or C3PA by adsorption at equivalence with monospecific antisera. The chemotactic response of these stimulated PMN was defective, suggesting altered membrane function.