MODULATION OF IMMUNE CELL-PROLIFERATION BY GLYCEROL MONOLAURATE

Previous studies have shown that glycerol monolaurate (GML), a surfact ant commonly used in a wide variety of food and cosmetic products, inh ibits the production of a variety of exotoxins by group A streptococci and staphylococci. Given the highly lipophilic nature of the structur e of GML, it is suspected that the surfactant exerts its toxin inhibit ion effects via interaction with the cell membrane. The present study attempted to characterize some of the potential targets of GML action using the model system of lymphocyte activation. Results from murine s plenocytes show that GML stimulates proliferation at concentrations be tween 10(-5) and 5 mu g/ml/5 x 10(5) splenocytes. At concentrations gr eater than 5 mu g/ml, GML inhibited lymphocyte proliferation and block ed the proliferative effects of the lymphocyte mitogens phorbol myrist ate acetate and concanavalin A and the potent T-cell mitogen toxic sho ck syndrome toxin-l, Studies using purified immune cell subsets indica ted that GML at a concentration of 0.1 mu g/ml optimally induced proli feration of T cells but did not affect B cells, At higher concentratio ns, CML inhibited the toxic shock syndrome toxin-1 mitogenic effects o n T cells, but did not inhibit the lipopolysaccharide-induced stimulat ion of B cells, suggesting that CML preferentially affects the T-cell population. GML-induced proliferation was blocked by the immunosuppres sive drug cyclosporin A, suggesting that GML may be exerting its T-cel l-proliferative effects along the calcium-dependent inositol phospholi pid signal transduction pathway.