Chemotactic deactivation of human neutrophils: possible relationship to stimulation of oxidative metabolism

Abstract

Neutrophils preexposed to high concentrations of activated complement or synthetic N-formyl methionyl peptides were inhibited in their subsequent spontaneous and chemotactic migratory responses. The possibility was considered that a part of this nonspecific loss of migratory function may be attributable to the interaction of the leukocytes with reactive forms of O2 deriving from the cytotoxin-induced burst of oxidative metabolic activity. The effect of preexposure of neutrophils from patients with chronic granulomatous disease to cytotoxins on their subsequent migratory responses was assessed. These responses were not altered by preexposure to either cytotoxin. There appeared to be a functional relationship between deactivation and the ability of the normal neutrophil to undergo a cytotoxin-induced respiratory burst.