抄録
To study the function and mechanism of eosinophils via the low affinity IgE receptor (Fc∈Rll), we examined the production of O2 metabolites by measuring the luminol-dependent chemiluminescence (LDCL) response and the generation of cysteinyl leukotrienes. Eosinophils obtained from guinea pig peritoneal fluid sensitized with horse serum were purified. Luminoldependent chemiluminescence was induced by stimulation with monoclonal anti-CD23 antibody, but not by mouse serum (controls). The mean (±SEM) value of LDCL was 20.6±1.3×103c.p.m. This reaction consisted of an initial rapid phase and a propagation phase and ended within 10min. Guinea pig eosinophils were histochemically stained with monoclonal anti-CD23 antibody. The major product generated in the LDCL response was superoxide, as determined by the measurement of superoxide by cytochrome c reduction and the complete inhibitory effect of superoxide dismutase on the LDCL response. Pretreatment with either pertussis toxin or cholera toxin inhibited the LDCL reaction. Depletion of bivalentions by EDTA inhibited this response and the protein kinase C inhibitor D-sphingosin inhibited both 1-oleoyl-2-acetyl-glycerol-induced and Fc∈Rll-mediated LDCL. These findings suggest that the NADPH-protein kinase C pathway may be involved in the Fc∈Rll-mediated LDCL response in guinea pig eosinophils.
