RELEASE OF PLATELET-ACTIVATING FACTOR (PAF-ACETHER) FROM ALVEOLAR MACROPHAGES BY THE CALCIUM IONOPHORE A 23187 AND PHAGOCYTOSIS
RELEASE OF PLATELET-ACTIVATING FACTOR (PAF-ACETHER) FROM ALVEOLAR MACROPHAGES BY THE CALCIUM IONOPHORE A 23187 AND PHAGOCYTOSIS
复制标题
DOI：
10.1111/j.1365-2362.1980.tb02082.x
复制
发表时间：
1980-01-01
影响因子：
5.5
通讯作者：
BENVENISTE, J
中科院分区：
文献类型：
--
作者：
ARNOUX, B;DUVAL, D;BENVENISTE, J
用钙离子载体A23187刺激兔、大鼠和人肺泡巨噬细胞，回收血小板活化因子(PAF-acether)。在酵母多糖存在下，大鼠和兔巨噬细胞也能释放PAF-乙醚，但人肺泡巨噬细胞有吞噬活性，但不能释放PAF-乙醚。观察到的释放是活跃的，依赖于钙离子，并在45分钟时处于平稳状态。从巨噬细胞冲出的肺中没有PAF-乙醚释放，这是反对这种介体起源于肥大细胞的另一个论点。鉴于PAF-乙醚具有强大的支气管收缩活性，其从肺泡巨噬细胞释放出来可能为非IgE依赖型哮喘和血小板在肺部疾病中的意义提供了另一种解释。
Platelet-activating factor (PAF-acether) was recovered from rabbit, rat and human alveolar macrophages stimulated with the Ca2+ ionophore A23187. PAF-acether release was also obtained from rat and rabbit macrophages in the presence of zymosan, but not from human alveolar preparations in spite of the phagocytic activity exhibited by the latter cells. Observed releases were active, Ca2+ dependent, and plateaued at 45 min. No PAF-acether was released from lungs washed out of their macrophages, another argument against the mastocyte origin of this mediator. Given the potent bronchoconstrictive activity of PAF-acether, its release from alveolar macrophages may provide an alternative explanation for non IgE-dependent asthmas and the implication of platelets in pulmonary diseases.