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Neutrophils synthesize reduced oxygen metabolites in response to chemoattractants that induce phagocytosis, respiratory burst, and degranulation. Antimicrobial and inflammatory agents that stimulate neutrophils also induce the enzyme NADPH oxidase, which produces superoxide (.O2-). To investigate the mechanisms of regulation of.O2- formation we measured.O2- formation induced by chemotactic peptide in several preparations of neutrophils from patients with chronic granulomatous disease (CGD), patients with X-linked chronic granulomatous disease, patients with normal neutrophil function, and in normal neutrophils obtained from healthy donors. Respiratory burst oxidase activity in these preparations of neutrophils was also measured. Basal.O2- production in CGD neutrophils was increased when compared with normal donor cells. In addition, chemotactic peptide-induced.O2- production was less in CGD neutrophils than in normal donor cells. X-linked chronic granulomatous disease neutrophils produced similar levels of.O2- in response to neutrophil chemotactic peptide as normal neutrophils. Neutrophils obtained from patients with normal neutrophil function also had decreased chemotactic peptide-induced.O2- production. Chemotactic peptide-induced respiratory burst oxidase activity was decreased in CGD and X-linked chronic
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