The influence of Staphylococcus aureus on peripheral blood lymphocytes (PBL) of patients with atopic dermatitis (AD) was analysed. The parameters studied were spontaneous and interleukin-inducible immunoglobulin (IgA, IgE, IgG) synthesis, as well as CD23 expression. Various heat-killed, clinical isolates of S. aureus were analysed. PBL from non-atopic donors served as controls. The time-course of co-cultured PBL with S. aureus showed a dose-dependent increase in immunoglobulin (Ig) synthesis from PBL of normal donors, whereas the Ig synthesis of atopic cells was significantly depressed. Additional stimulation with interleukin-4 (IL-4) also led to a pronounced suppression of the IgE and IgA synthesis in normal donor cells, while the effect of S. aureus on PBL of atopic donors was not markedly affected by IL-4. Transwell cultures of bacteria separated from PBL by a semi-permeable membrane induced stimulation of IgA and IgE synthesis in patients with AD. The Ig synthesis in the control group was not altered. Co-stimulation of S. aureus and IL-4 in this system led to a suppression of IgA with cells of both atopic and normal donors. IgE synthesis from atopic PBL was significantly stimulated. The CD23 expression of atopic PBL was increased by S. aureus and IL-4. Our data indicate that S. aureus may modulate the cytokine-dependent humoral immunity in patients with AD and that chronic colonization of the skin may be responsible for allergic skin reactions in AD.