Interactions of Granulocyte - Macrophage Colony - Stimulating Factor ( CSF ) , Granulocyte CSF , and Tumor Necrosis Factor a in the Priming of the Neutrophil Respiratory Burst

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 C5astimulated neutrophil H,O, 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 a (TNFa) produced a similar degree of priming of the FMLP-stimulated burst in vitro (558% +. 86%. n = 41, and 581% f 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 faetor (G-CSF) alone caused only modest priming (202% f 39%, n = 14). Priming with cytokine combinations of the FMLP-stimulated burst showed that the combinations of G-CSF and TNFa and GM-CSF and TNFa are highly synergistic, with recruitment of neutrophils