Inhibition of neutrophil functions by human immunoglobulin E.

Incubation of human neutrophils with human immunoglobulin (Ig) E caused dose-dependent inhibition of adhesion, phagocytosis, secretion of myeloperoxidase, and oxygen radical production. The concentrations of IgE that caused 50% inhibition of adhesion, phagocytosis, and secretion were 2 +/- 0.3, 2.16 +/- 0.21, and 1.95 +/- 0.28 ng/ml, respectively. Oxidase activation as measured by luminol-dependent chemiluminescence by the receptor-mediated N-formyl-methionyl-leucyl-phenylalanine, phorbol 12-myristate 13-acetate, or the particulate stimulus Staphylococcus aureus was inhibited by IgE with concentrations causing 50% effect of 1.2 +/- 0.13, 1.09 +/- 0.16, and 0.6 +/- 0.09 ng/ml, respectively. IgE also inhibited oxygen consumption rate and cytochrome c reduction with similar K0.5 values. The effect of IgE was unlikely to be due to nonspecific cytotoxicity because trypan blue exclusion test and the cytoplasmic marker lactate dehydrogenase revealed that the cells retained their viability after IgE treatment. Similar or higher concentrations of IgG invoked either no inhibition or a slight enhancement of neutrophil functions. Pretreatment of neutrophils with IgG failed to affect the IgE-induced inhibition. Because the effect of IgE occurs at concentrations less than those reported in hyperimmunoglobulinemia E, we propose that direct inhibition of neutrophil functions may underlie the pathogenesis of recurrent infection associated with hyperimmunoglobulinemia E.