RECOMBINANT BOVINE GM-CSF PRIMES SUPEROXIDE PRODUCTION BUT NOT DEGRANULATION INDUCED BY RECOMBINANT BOVINE INTERLEUKIN-1-BETA IN BOVINE NEUTROPHILS

Bovine neutrophil activation, superoxide production, and beta-glucosam inadase release induced by various biological stimuli were examined. P latelet-activating factor (PAF) and recombinant bovine interleukin-1be ta (r-BoIL-1beta) induced superoxide production and beta-glucosaminada se release in bovine neutrophils. When these two responses were compar ed, the dose requirement for maximum activation was similar for PAF (1 X 10(-6) M). However, the concentration of r-BoIL-1beta required for the maximum degranulation (2.5 X 10(-7) M) was 100-fold higher than th at for the maximum superoxide production (2.5 x 10(-9) M). Furthermore , pretreatment of cells with recombinant bovine granulocyte-macrophage colony-stimulating factor (r-BoGM-CSF) enhanced both superoxide produ ction and beta-glucosaminidase release induced by PAF. In contrast, wh ereas superoxide production induced by r-BoIL-1beta was enhanced by r- BoGM-CSF priming, beta-glucosaminidase release induced by r-BoIL-1beta was significantly reduced by pretreatment with r-BoGM-CSF. CL 184,005 , a PAF antagonist, inhibited PAF-induced glucosaminidase release and superoxide production but did not inhibit r-BoIL-1beta-induced superox ide production and degranulation. In addition, it did not inhibit the priming effect of r-BoGM-CSF on r-BoIL-1beta-induced superoxide produc tion. These results suggest that (1) PAF and r-BoIL-1beta activate bov ine neutrophils by different mechanisms, (2) r-BoGM-CSF primes superox ide production and degranulation induced by PAF, (3) r-BoGM-CSF primes superoxide production but not degranulation induced by r-BoIL-1beta, and (4) the priming effect of r-BoGM-CSF is not mediated by PAF.