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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Modulation of immune cell proliferation by glycerol monolaurate.
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Modulation of immune cell proliferation by glycerol monolaurate.

机译：单月桂酸甘油酯对免疫细胞增殖的调节。

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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.
机译：先前的研究表明，甘油单月桂酸酯（GML）是一种广泛用于各种食品和化妆品中的表面活性剂，可抑制A组链球菌和葡萄球菌产生多种外毒素。鉴于GML结构的高度亲脂性，人们怀疑表面活性剂会通过与细胞膜的相互作用发挥其毒素抑制作用。本研究试图使用淋巴细胞活化模型系统表征某些GML作用的潜在靶标。鼠脾细胞的结果表明，GML在10（-5）和5微克/ ml / 5 x 10（5）脾细胞之间的浓度刺激增殖。在浓度大于5微克/毫升时，GML抑制淋巴细胞增殖并阻断淋巴细胞有丝分裂原醋酸佛波醇肉豆蔻酸酯乙酸和伴刀豆球蛋白A的增殖作用以及强效的T细胞有丝分裂原毒性休克综合征毒素1。使用纯化的免疫细胞亚群的研究表明，浓度为0.1微克/毫升的GML可以最佳地诱导T细胞增殖，但不会影响B细胞。在较高浓度下，GML抑制了毒性休克综合征毒素1对T细胞的促有丝分裂作用，但没有抑制脂多糖诱导的B细胞刺激，提示GML优先影响T细胞群体。 GML诱导的增殖被免疫抑制药物环孢菌素A阻断，表明GML可能沿着钙依赖性肌醇磷脂信号转导途径发挥其T细胞增殖作用。

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