Modulation of immune cell proliferation by glycerol monolaurate.
Previous studies have shown that glycerol monolaurate (GML), a surfactant commonly used in a wide variety of food and cosmetic products, inhibits the production of a variety of exotoxins by group A streptococci and staphylococci. Given the highly lipophilic nature of the structure of GML, it is suspected that the surfactant exerts its toxin inhibition 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 splenocytes show that GML stimulates proliferation at concentrations between 10(-5) and 5 micrograms/ml/5 x 10(5) splenocytes. At concentrations greater than 5 micrograms/ml, GML inhibited lymphocyte proliferation and blocked the proliferative effects of the lymphocyte mitogens phorbol myristate acetate and concanavalin A and the potent T-cell mitogen toxic shock syndrome toxin-1. Studies using purified immune cell subsets indicated that GML at a concentration of 0.1 microgram/ml optimally induced proliferation of T cells but did not affect B cells. At higher concentrations, GML inhibited the toxic shock syndrome toxin-1 mitogenic effects on T cells, but did not inhibit the lipopolysaccharide-induced stimulation of B cells, suggesting that GML preferentially affects the T-cell population. GML-induced proliferation was blocked by the immunosuppressive drug cyclosporin A, suggesting that GML may be exerting its T-cell-proliferative effects along the calcium-dependent inositol phospholipid signal transduction pathway.
Witcher
K J
KJ
Department of Microbiology, University of Minnesota Medical School, Minneapolis 55455, USA.
Novick
R P
RP
Schlievert
P M
PM
D000818:Animals; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology; D001427:Bacterial Toxins; D002462:Cell Membrane / Q000187:drug effects / Q000276:immunology; D003208:Concanavalin A / Q000494:pharmacology; D016572:Cyclosporine / Q000494:pharmacology; D004768:Enterotoxins / Q000494:pharmacology; D005260:Female; D005989:Glycerides / Q000494:pharmacology*; D007166:Immunosuppressive Agents / Q000494:pharmacology; D066298:In Vitro Techniques; D007376:Interleukin-2 / Q000276:immunology; D007848:Laurates / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D008934:Mitogens / Q000494:pharmacology; D050178:Monoglycerides; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D018089:Superantigens; D013501:Surface-Active Agents / Q000494:pharmacology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D001427:Bacterial Toxins; D004768:Enterotoxins; D005989:Glycerides; D007166:Immunosuppressive Agents; D007376:Interleukin-2; D007848:Laurates; D008070:Lipopolysaccharides; D008934:Mitogens; D050178:Monoglycerides; D018089:Superantigens; D013501:Surface-Active Agents; C030107:enterotoxin F, Staphylococcal; D003208:Concanavalin A; C020777:monolaurin; D016572:Cyclosporine; D013755:Tetradecanoylphorbol Acetate