Schnyder J, Dewald B, Baggiolini M
Prostaglandins. 1981 Sep;22(3):411-21. doi: 10.1016/0090-6980(81)90102-7.
The effect of the cyclooxygenase inhibitors, indomethacin and diclofenac, and of PGE2 on either resting or stimulated macrophages was investigated. Peritoneal macrophages were obtained from untreated mice and cultured for 10 days. Macrophage activation was induced by zymosan phagocytosis and was monitored by testing for plasminogen activator secretion and the cellular levels of lactate dehydrogenase, beta-glucuronidase and alkaline phosphodiesterase I. It was found that cyclooxygenase inhibitors activate resting macrophages and enhance the degree of activation obtained after zymosan phagocytosis. Addition of exogenous PGE2, on the other hand, had the opposite effect, it suppressed activation induced either by cyclooxygenase inhibitors, phagocytosis or a combination of both. Cyclooxygenase inhibitors and PGE2 did not affect the hexose monophosphate shunt activity of resting macrophages and had only a minor effect on the respiratory burst occurring during zymosan phagocytosis. It appears, therefore, that the observed changes in the state of activation of the macrophages are not related to hexose monophosphate shunt activity. The described effects suggest that PGE2 and possibly other cyclooxygenase products may function as inhibitory feed-back regulators of macrophage activation.
研究了环氧化酶抑制剂吲哚美辛和双氯芬酸以及前列腺素E2对静息或受刺激巨噬细胞的影响。从未经处理的小鼠获取腹腔巨噬细胞，并培养10天。通过酵母聚糖吞噬诱导巨噬细胞活化，并通过检测纤溶酶原激活物分泌以及乳酸脱氢酶、β-葡萄糖醛酸酶和碱性磷酸二酯酶I的细胞水平进行监测。发现环氧化酶抑制剂可激活静息巨噬细胞，并增强酵母聚糖吞噬后获得的活化程度。另一方面，添加外源性前列腺素E2则产生相反的效果，它抑制由环氧化酶抑制剂、吞噬作用或两者组合诱导的活化。环氧化酶抑制剂和前列腺素E2不影响静息巨噬细胞的磷酸己糖旁路活性，对酵母聚糖吞噬过程中发生的呼吸爆发也只有轻微影响。因此，看来观察到的巨噬细胞活化状态变化与磷酸己糖旁路活性无关。所述效应表明，前列腺素E2以及可能的其他环氧化酶产物可能作为巨噬细胞活化的抑制性反馈调节因子发挥作用。
