HUMAN RECOMBINANT GM-CSF SELECTIVELY PRIMES RECEPTOR-MEDIATED RESPIRATORY BURST OF NEUTROPHILS IN-VITRO

The influence of human recombinant granulocyte-macrophage colony-stimu lating factor (rH GM-CSF) on respiratory burst response of isolated hu man neutrophils was examined. Preincubation of cells with rH GM-CSF si gnificantly increased the respiratory burst in response to formyl-meth ionyl-leucyl-phenylalanine (FMLP), measured by luminol-dependent chemi luminescence (CL) assay. This priming effect of rH GM-CSF was independ ent of extracellular Ca2+ and Mg2+. On the other hand, the pretreatmen t of cells with rH GM-CSF could not enhance the neutrophil CL response s to unopsonized, serum complement-opsonized or immunoglobulin G (IgG) -opsonized zymosan particles. rH GM-CSF directly induced a weak CL sig nal in neutrophils. This signal, however, was abolished when extra-cel lular Ca2+ and Mg2+ were removed. Exposure to rH GM-CSF caused a dival ent cation-dependent up-regulation of complement receptors (CR1 and CR 3) on neutrophil cell surface, while the expression of IgG Fc-receptor s (FcRII and FcRIII) was not markedly changed by rH GM-CSF. The result s indicate that rH GM-CSF primes FMLP-induced CL but not zymosan parti cle-induced respiratory burst in human neutrophils. It is hypothesized that the reason for the different sensitivity of FMLP-receptors and r eceptors to zymosan particles to rH GM-CSF priming may lie in differen ces in the signal-transduction pathways of these receptor types.