Human recombinant GM-CSF selectively primes receptor mediated respiratory burst of neutrophils in vitro.

Abstract

The influence of human recombinant granulocyte-macrophage colony-stimulating factor (rH GM-CSF) on respiratory burst response of isolated human neutrophils was examined. Preincubation of cells with rH GM-CSF significantly increased the respiratory burst in response to formyl-methionyl-leucyl-phenylalanine (FMLP), measured by luminol-dependent chemiluminescence (CL) assay. This priming effect of rH GM-CSF was independent of extracellular Ca2+ and Mg2+. On the other hand, the pretreatment of cells with rH GM-CSF could not enhance the neutrophil CL responses to unopsonized, serum complement-opsonized or immunoglobulin G (IgG)-opsonized zymosan particles. rH GM-CSF directly induced a weak CL signal in neutrophils. This signal, however, was abolished when extracellular Ca2+ and Mg2+ were removed. Exposure to rH GM-CSF caused a divalent cation-dependent up-regulation of complement receptors (CR1 and CR3) on neutrophil cell surface, while the expression of IgG Fc-receptors (FcRII and FcRIII) was not markedly changed by rH GM-CSF. The results indicate that rH GM-CSF primes FMLP-induced CL but not zymosan particle-induced respiratory burst in human neutrophils. It is hypothesized that the reason for the different sensitivity of FMLP-receptors and receptors to zymosan particles to rH GM-CSF priming may lie in differences in the signal-transduction pathways of these receptor types.