High affinity IgE receptor (Fc epsilon R I) expression on monocytes and its upregulation on monocytes from patients with atopic dermatitis (AD) have been recently reported. In this study, we investigated whether prostaglandin E2 (PGE2) release from AD monocytes was Fc epsilon R I-dependent or not. The monocytes were stimulated with anti-Fc epsilon R I monoclonal antibody (mAb) and anti-Fc epsilon R II mAb. Cross-linking of Fc epsilon R I, but not that of Fc epsilon R II induced PGE2 release from monocytes. In order to confirm that the PGE2 release is IgE-dependent, stimulation with IgE+anti-IgE, IgG+anti-IgG and immune complexes made by incubation with AD patients' serum and recombinant Der fII (rDer fII-IC) were carried out in the culture. Significant PGE2 release by all the stimulants was observed, as compared with spontaneous release. PGE2 release by immune complex made by incubation with IgE-absorbed AD serum and rDer fII was much lower than that by rDer fII-IC. In monocytes from nonatopic donors, significant PGE2 release was observed when stimulated with IgE+anti-IgE, IgG+anti-IgG, rDer fII-IC, but not with anti-FC epsilon R I mAb and anti-Fc epsilon R II mAb. However, the release were significantly lower than respective PGE2 releases from AD monocytes. Taken together, cross-linking of Fc epsilon R I and IgE induced a PGE2 release from monocytes. This is a first report demonstrating an Fc epsilon R I-dependent mediator release from monocytes of AD patients.