IgE produces monocyte superoxide anion release: correlation with CD23 expression. Comparison of patients with asthma, patients with rhinitis, and normal subjects.

Allergic inflammation involves many different cell types among which mononuclear cells, such as macrophages and monocytes, play an important role. These cells release numerous chemical mediators, including superoxide anion (O2.-). We evaluated the capacity of atopic serum to stimulate peripheral blood monocyte O2.- release. Thirteen untreated allergic patients (seven with asthma and six with rhinitis), and five nonallergic control subjects were studied. O2.- was measured in a photon-counting camera with Lucigenin-enhanced (Sigma Chemical Co., St. Louis, Mo.) chemiluminescence. Results were expressed (mean +/- SEM) in relation to basal values (peak/basal chemiluminescence values). Spontaneous production of O2.- was greater in allergic patients. Moreover, atopic serum stimulated O2.- production of blood monocytes in all subjects, but this was greater in subjects with allergic asthma than in subjects with allergic rhinitis and normal subjects. Anti-IgE immunoadsorption of atopic serum completely abrogated this effect, which was restored by the IgE-rich eluted fraction. IgE-induced O2.- release decreased as adherence duration increased and was correlated with surface CD23 expression. These results indicate that monocytes from allergic patients are in an activated state and that binding of IgE to their receptors generates O2.-, possibly by direct activation of blood monocyte reduced nicotinamide adenine dinucleotide phosphate oxidase.