Fernández-Repollet E, Mittler R S, Tiffany S, Schwartz A
J Histochem Cytochem. 1982 May;30(5):466-70. doi: 10.1177/30.5.6804558.
Several studies have suggested that prostaglandin E2 (PGE2) might influence the phagocytic activity of macrophage cells. The present study was designed to examine the in vivo effects of PGE2, the prostaglandin synthesis inhibitor meclofenamate, the prostaglandin precursor arachidonic acid, and the biologically inactive fatty acid 11,14,17-eicosatrienoic acid on phagocytosis by peritoneal macrophage cells in the rat. Following 3 days of treatment with either agent, fluorescent methacrylate microbeads were injected intraperitoneally into all rats. Peritoneal exudates were harvested after administration of the microbeads and the percent phagocytosis determined in macrophage cells using a fluorescence-activated cell sorter (FACS II). The administration of PGE2 was associated with a significant decrease in the percentage of peritoneal macrophages ingesting the fluorescent methacrylate microbeads. In contrast, treatment with arachidonic acid or 11,14,17-eicosatrienoic acid significantly enhanced the percentage of phagocytic macrophage cells. A significant increase in the number of macrophages undergoing phagocytosis of the methacrylate microbeads was also observed in rats treated with meclofenamate. This later observation, taken together with the inhibitory effect induced by PGE2 on macrophage phagocytosis, points to a potential modulator role of PGE2 on the phagocytic activity of macrophages. These data also suggest that arachidonic acid might influence macrophage phagocytosis by a mechanism independent of PGE2.
多项研究表明,前列腺素E2(PGE2)可能会影响巨噬细胞的吞噬活性。本研究旨在检测PGE2、前列腺素合成抑制剂甲氯芬那酸、前列腺素前体花生四烯酸以及生物活性脂肪酸11,14,17-二十碳三烯酸对大鼠腹膜巨噬细胞吞噬作用的体内影响。用任何一种药物处理3天后,将荧光甲基丙烯酸酯微珠腹腔注射到所有大鼠体内。注射微珠后收集腹膜渗出液,并使用荧光激活细胞分选仪(FACS II)测定巨噬细胞中的吞噬百分比。PGE2的给药与摄取荧光甲基丙烯酸酯微珠的腹膜巨噬细胞百分比显著降低有关。相反,用花生四烯酸或11,14,17-二十碳三烯酸处理可显著提高吞噬性巨噬细胞的百分比。在用甲氯芬那酸处理的大鼠中,还观察到吞噬甲基丙烯酸酯微珠的巨噬细胞数量显著增加。这一最新观察结果,连同PGE2对巨噬细胞吞噬作用的抑制作用,表明PGE2对巨噬细胞的吞噬活性具有潜在的调节作用。这些数据还表明,花生四烯酸可能通过一种独立于PGE2的机制影响巨噬细胞的吞噬作用。