[Isotypic regulation of antibodies and antibiotics]

Several reports have shown that antibiotics can in vitro interfere with many aspects of the immune response such as phagocytic processes, macrophage functions, T and B cell proliferation. Very few data on the effect of antibiotics on the antibody response were available. It is well known that the humoral immune response is sustained by different immunoglobulin isotypes (IgA, IgE, IgG or IgM) according to the antigen, its penetration route, the mucosal-associated lymphoid tissue, the genetic background and the age of the host. Such an isotypic regulation was very recently demonstrated to be closely related to some cytokines like interferon-gamma, interleukins (IL)-2, -4 and -10. We tested the effect of some cephalosporins on in vitro cytokine-dependent immunoglobulin production. Neither cefadroxil nor cefalexine had any modulating effect on pokeweed mitogen-induced IgG and IgM production by normal human B-cells. In contrast, cefadroxil, and not cefalexine, blocked up to 90% of the in vitro IL-4-dependent IgE production by normal B lymphocytes. In the same way, this cephalosporin was able to inhibit the membrane expression of CD23 molecules (low affinity Fc-epsilon-receptors) which is involved in phagocytic processes and in IgE regulation. The first target cell of the effect of cefadroxil was clearly shown to be monocyte-macrophage lineage which were stimulated to produce prostaglandin E2 which down regulated CD23 membrane expression and IgE secretion. Such data showed that antibiotics were able to interfere with cytokine cascade which controlled the immunoglobulin isotype.