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Research Article Free access | 10.1172/JCI109346

Fluoride-mediated activation of the respiratory burst in human neutrophils. A reversible process.

J T Curnutte, B M Babior, and M L Karnovsky

Find articles by Curnutte, J. in: JCI | PubMed | Google Scholar

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Published April 1, 1979 - More info

Published in Volume 63, Issue 4 on April 1, 1979
J Clin Invest. 1979;63(4):637–647. https://doi.org/10.1172/JCI109346.
© 1979 The American Society for Clinical Investigation
Published April 1, 1979 - Version history
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Abstract

Fluoride ion (F-) is an effective activator of the respiratory burst in neutrophils, as indicated by its ability to induce O2- production by these cells. Other halide ions did not activate the burst, Cl-, in particular appeared to antagonize the effect of F- on O2- production. F- stimulated O2- production showed a requirement for Ca++, but was independent of other exogenous cations. Neither phagocytosis nor degranulation were necessary for respiratory burst activation by F-. The effect of F- on the respiratory burst was reversible. Washing the cells after treatment with F-, while they were still producing large amounts of O2-, returned them to the resting state. They could then be stimulated again to produce O2- in amounts equivalent to those originally produced. Our experiments indicated that restimulation did not represent the activation of a population of cells that had not been activated during the initial exposure to F-, nor did it represent serial activation of different subpopulation of the O2- forming enzyme molecules present in a given cell. Rather, our data suggest that the entire population of O2- forming enzyme molecules was activated in a reversible fashion by F-.

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