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Interactions of granulocyte-macrophage colony-stimulating factor (CSF),
granulocyte CSF, and tumor necrosis factor alpha in the priming of the
neutrophil respiratory burst
A Khwaja, JE Carver and DC Linch
Department of Haematology, University College and Middlesex School of
Medicine, London, UK.
Exposure of neutrophils to a range of cytokines augments their response to
subsequent agonist-induced activation of the respiratory burst. We have
examined the effects of several of these factors, both singly and in
combination, on the priming of f-met-leu-phe (FMLP) and complement
C5a-stimulated neutrophil H2O2 production, using a whole blood flow
cytometric assay designed to minimize artefactual activation. Both
granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor
necrosis factor alpha (TNF alpha) produced a similar degree of priming of
the FMLP-stimulated burst in vitro (558% +/- 86%, n = 41, and 581% +/- 95%,
n = 21, of the response seen with FMLP alone, respectively), but with
markedly different kinetics (half-maximal response 20 minutes and 7
minutes, respectively). Preincubation with granulocyte colony- stimulating
factor (G-CSF) alone caused only modest priming (202% +/- 39%, n = 14).
Priming with cytokine combinations of the FMLP-stimulated burst showed that
the combinations of G-CSF and TNF alpha and GM-CSF and TNF alpha are highly
synergistic, with recruitment of neutrophils unresponsive to priming by
single agents. Priming with the combination of GM-CSF and G-CSF was not
significantly different to priming with GM- CSF alone. Similar results were
obtained using C5a as the respiratory burst stimulus. Significant priming
of the FMLP-stimulated respiratory burst was seen in vivo in patients
receiving an infusion of GM-CSF (332% +/- 50% of preinfusion response to
FMLP, P less than .005, n = 8). Priming was also seen in patients receiving
G-CSF (152% +/- 58%, n = 5), although this did not reach conventional
significance levels (.05 less than P less than .1). Although GM-CSF
infusion caused priming in vivo, this was 48% less than predicted by
preinfusion in vitro responses. This result was not due to inadequate
GM-CSF levels as addition of further GM-CSF ex vivo did not correct the
response. However, these neutrophils were still able to respond
appropriately to ex vivo priming with TNF alpha, with a doubling in H2O2
production.
Volume 79,
Issue 3,
pp. 745-753,
02/01/1992
Copyright © 1992 by The American Society of Hematology
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