Prostaglandin D2 generation after activation of rat and human mast cells with anti-IgE.
Prostaglandin D2 generation after activation of rat and human mast cells with anti-IgE.
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DOI：
10.4049/jimmunol.129.4.1627
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发表时间：
1982-10
影响因子：
4.4
通讯作者：
R. Lewis;N. Soter;P. Diamond;K. Austen;J. Oates;L. Roberts
中科院分区：
文献类型：
--
作者：
R. Lewis;N. Soter;P. Diamond;K. Austen;J. Oates;L. Roberts
大鼠和人肥大细胞的抗IgE依赖激活导致环氧合酶产物前列腺素D2(PGD2)和前列腺素I2(PGI2)在大鼠和人体内优先产生。用气相色谱-质谱法测定，纯化的大鼠肥大细胞的平均净生成量为13.1 ng/10(6)，分散的富集人肥大细胞的净生成量为39.5 ng/10(6)。在IgE依赖的激活后，当肥大细胞数量变化但细胞总数保持不变时，分散的人肺细胞产生的PGD2净数量和组胺的分泌量之间存在线性关系，这表明决定PGD2生成的是参与IgE依赖激活的肥大细胞数量，而不是肥大细胞总数。放射免疫法测定的PGD2生成量与纯化的大鼠肥大细胞释放颗粒标志物β-氨基己糖苷酶在其对抗-IgE刺激反应的剂量-反应部分之间也呈线性关系。随着抗-IgE浓度的升高，大鼠肥大细胞产生PGD2的量趋于平稳，而净释放的β-己糖氨酸酶百分比进一步增加。在用抗IgE激活的大鼠肥大细胞的动力学研究中，相对于β-己糖苷酶的开始释放(15~30秒)和完成释放(1~2分钟)，PGD2的开始(1~2分钟)和最大生成时间(5~10分钟)被推迟。因此，在IgE依赖的肥大细胞激活过程中，PGD2在细胞外的出现代表了对颗粒相关介质分泌的额外反应。
Anti-IgE-dependent activation of rat and human mast cells resulted in the preferential generation of the cyclooxygenase products prostaglandin D2 (PGD2) and prostaglandin I2 (PGI2) in the rat and PGD2 in the human. The average net generation of PGD2, determined by gas chromatography-mass spectrometry, was 13.1 ng/10(6) purified rat mast cells and 39.5 ng/10(6) dispersed, enriched human mast cells. After IgE-dependent activation, there was a linear relationship between the net quantities of PGD2 generated and of histamine secreted from dispersed human pulmonary cells when the number of mast cells was varied but the total number of cells was held constant, indicating that it is the number of mast cells participating in IgE-dependent activation, rather than total mast cell number, that determines PGD2 generation. A linear relationship was also shown between PGD2 generation, determined by radioimmunoassay, and the release of the granule marker beta-hexosaminidase from purified rat mast cells on the dose-response portion of the plot of their response to anti-IgE challenge. With higher concentrations of anti-IgE, PGD2 generation from rat mast cells plateaued, whereas net percent beta-hexosaminidase release increased further. In kinetic studies of rat mast cells activated with anti-IgE, the onset (1 to 2 min) and time of maximum generation (5 to 10 min) for PGD2 were delayed relative to the onset (15 to 30 sec) and completion (1 to 2 min) of beta-hexosaminidase release. Thus, the extracellular appearance of PGD2 during IgE-dependent mast cell activation represents a response additional to the secretion of granule-associated mediators.