VERY LOW-DENSITY LIPOPROTEINS (VLDL) TRIGGER THE RELEASE OF HISTAMINE FROM HUMAN BASOPHILS
VERY LOW-DENSITY LIPOPROTEINS (VLDL) TRIGGER THE RELEASE OF HISTAMINE FROM HUMAN BASOPHILS
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DOI：
10.1016/0005-2760(87)90121-4
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发表时间：
1987-02-23
期刊：
影响因子：
--
通讯作者：
SCHULMAN, ES
中科院分区：
文献类型：
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作者：
GONEN, B;ODONNELL, P;SCHULMAN, ES
循环嗜碱性粒细胞是颗粒相关介质组胺的公认来源。然而，对人体嗜碱性粒细胞释放组胺的生理控制知之甚少。由于组胺可能发挥作用的各种化合物，包括极低密度脂蛋白（VLDL）及其水解产物的transendothelial运输，我们调查的可能性，VLDL调节介质释放嗜碱性粒细胞。VLDL（生理浓度）与嗜碱性粒细胞（分离为混合白细胞制剂）孵育导致组胺显著释放。组胺的释放依赖于VLDL浓度（在VLDL-蛋白浓度为15-20 μ g/ml时出现半最大刺激）、温育时间（在5-12分钟时半最大释放）、温度（37 ℃）、温度（20 ℃）、温度（30 ℃）、温度（30 ℃）、温度（30 ℃）。C最佳）和所需的钙（浓度0.5-2.0 mM）。此外，VLDL诱导的组胺释放被三种不同的介质释放抑制剂抑制：二甲双胍，二丁酰cAMP和去甲二氢愈创木酸。在相同的实验条件下，嗜碱性粒细胞与LDL或HDL的孵育没有导致显着的组胺释放嗜碱性粒细胞。从不同供体获得的嗜碱性粒细胞的组胺分泌反应差异很大。从28个供体中分离的嗜碱性粒细胞用100 μ g/ml VLDL攻击释放23 ± 0.001 μ g/ml。5%的细胞组胺（平均值± 0.001）。S.E.;范围为0-94%）。VLDL诱导的组胺释放的脱敏可以通过将嗜碱性粒细胞与VLDL或抗IgE预孵育来完成，但不能与N-甲酰基-L-甲硫氨酰-L-亮氨酰-L-苯丙氨酸预孵育。通过分泌组胺，一种有效的血管活性介质（也可能通过颗粒相关的糖胺聚糖，脂蛋白脂肪酶的刺激物），这种VLDL的新作用可能是调节VLDL水解和脂质转运的生理回路的一部分。由于组胺的致动脉粥样硬化特性，VLDL的这种作用也可能具有有害的后果。
Circulating basophils are well established sources of the granule-associated mediator, histamine. The physiological control, however, of histamine release from human basophils is poorly understood. Because histamine may play a role in the transendothelial transport of various compounds, including very low density lipoprotein (VLDL) and its hydrolysis products, we investigated the possibility that VLDL regulates mediator release from basophils. The incubation of VLDL (at physiological concentrations) with basophils (isolated as mixed leukocyte preparations) resulted in a significant release of histamine. Histamine release was dependent on VLDL concentration (half-maximal stimulation occurring at VLDL-protein concentration of 15-20 .mu.g/ml), length of incubation (half-maximal release at 5-12 min), temperature (37.degree. C optimum) and required calcium (concentation 0.5-2.0 mM). Furthermore, VLDL-induced histamine release was inhibited by three different mediator-release inhibitors: dimaprit, dibutyryl cAMP and nordihydroguaiaretic acid. Incubation of basophils with LDL or HDL under the same experimental conditions did not result in significant histamine release from basophils. The histamine-secretory response of basophils obtained from different donors varied considerably. Basophils isolated from 28 donors and challenged with 100 .mu.g/ml VLDL released 23 .+-. 5% of their cellular histamine (mean .+-. S.E.; with a range of 0-94%). Desensitization of VLDL-induced histamine release could be accomplished by preincubation of basophils with either VLDL or anti-IgE but not with N-formyl-L-methionyl-L-leucyl-L-phenylalanine. Through the secretion of histamine, a potent vasoactive mediator (and also possibly through granule-associated glycosaminoglycans, stimulants of the enzyme lipoprotein lipase), this novel effect of VLDL may be part of a physiological loop for the regulation of VLDL hydrolysis and lipid transport. This effect of VLDL may also have deleterious consequences, because of the atherogenic properties of histamine.