Chemotactic deactivation of human neutrophils: possible relationship to stimulation of oxidative metabolism.
Neutrophils preexposed to high concentrations of activated complement or synthetic N-formyl methionyl peptides are inhibited in their subsequent spontaneous and chemotactic migratory responses. We have considered the possibility that a part of this nonspecific loss of migratory function may be attributable to the interaction of the leukocytes with reactive forms of oxygen deriving from the cytotaxin-induced burst of oxidative metabolic activity. For these studies we have assessed the effect of preexposure of neutrophils from patients with chronic granulomatous disease to cytotaxins on their subsequent migratory responses. We find that these responses are not altered by preexposure to either cytotaxin. Thus, there appears to be a functional relationship between deactivation and the ability of the normal neutrophil to undergo a cytotaxin-induced respiratory burst.
D001769:Blood; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D006105:Granulomatous Disease, Chronic / Q000097:blood; D006801:Humans; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*; D010101:Oxygen Consumption; D010455:Peptides / Q000494:pharmacology; D015054:Zymosan
D010455:Peptides; D015054:Zymosan