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Research Article Free access | 10.1172/JCI107594

Stimulation of human neutrophil leukocyte aerobic glucose metabolism by purified chemotactic factors.

E J Goetzl and K F Austen

Department of Medicine, Harvard Medical School and Robert B. Brigham Hospital, Boston, Massachusetts 02120, USA.

Find articles by Goetzl, E. in: PubMed | Google Scholar

Department of Medicine, Harvard Medical School and Robert B. Brigham Hospital, Boston, Massachusetts 02120, USA.

Find articles by Austen, K. in: PubMed | Google Scholar

Published February 1, 1974 - More info

Published in Volume 53, Issue 2 on February 1, 1974
J Clin Invest. 1974;53(2):591–599. https://doi.org/10.1172/JCI107594.
© 1974 The American Society for Clinical Investigation
Published February 1, 1974 - Version history
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Abstract

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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