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Research Article Free access | 10.1172/JCI107594
Department of Medicine, Harvard Medical School and Robert B. Brigham Hospital, Boston, Massachusetts 02120, USA.
Find articles by Goetzl, E. in: JCI | PubMed | Google Scholar
Department of Medicine, Harvard Medical School and Robert B. Brigham Hospital, Boston, Massachusetts 02120, USA.
Find articles by Austen, K. in: JCI | PubMed | Google Scholar
Published February 1, 1974 - More info
The interaction of human neutrophils adherent to plastic petri dishes with the purified chemotactic factors C5a and kallikrein increased their rate of aerobic glycolysis 25-120% and the activity of their hexose monophosphate shunt (HMPS) 100-600%, reaching a plateau after 2 hr at 37 degrees C. The stimulation of either pathway required a chemotactically active stimulus since neither C5 nor prekallikrein or inactivated kallikrein could enhance metabolic activity. Marked suppression of the neutrophil chemotactic response by preincubation with a chemotactic factor to achieve deactivation, 5 x 10(-7) M diisopropyl fluorophosphate, or the neutrophil immobilizing factor (NIF) did not prevent the stimulation of HMPS activity or glycolysis by chemotactic factors. The metabolic inhibitors iodoacetate and 6-aminonicotinamide at concentrations which blocked enhancement of glycolysis or HMPS activity, respectively, partially suppressed the chemotactic response of neutrophils to the chemotactic factors. The capacity of a chemotactic factor to stimulate glucose metabolism of human neutrophils is associated with a maximal chemotactic response, but this stimulation is not alone sufficient for chemotaxis.
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