Parnham M J, Winkelman J, Hartung H P, Hadding U
Agents Actions Suppl. 1984;14:215-26.
Macrophages, on stimulation, generate both cyclo-oxygenase and lipoxygenase products of arachidonic acid as well as the acetylated phospholipid, PAF-acether. The latter induces the oxidative burst in C. parvum-activated macrophages, but has little activity on resident macrophages. Mouse macrophages are generally rather insensitive to PAF-acether. Prostaglandin (PG)E2, on the other hand is a potent inhibitor of the macrophage oxidative burst, though its activity is also dependent upon the source of the macrophages and the stimulus used. Several lipoxygenase inhibitors inhibit the oxidative burst of mouse peritoneal macrophages, while other authors have reported stimulatory effects of lipoxygenase products on different macrophage populations. The differential actions of lipoxygenase and cyclo-oxygenase products on the macrophage oxidative burst are reflected by the effect of arachidonic acid on the zymosan induced response of mouse resident peritoneal cells: initial enhancement, followed by prolonged inhibition, the latter being indomethacin-sensitive. While PAF-acether is probably an important initiator of the macrophage oxidative burst in vivo, arachidonic acid modulates the response by a "see-saw mechanism", lipoxygenase products being stimulatory and cyclo-oxygenase products (mainly PGE2) being inhibitory.
巨噬细胞受到刺激后，会生成花生四烯酸的环氧化酶和脂氧化酶产物以及乙酰化磷脂——血小板激活因子（PAF-乙酰醚）。后者可诱导微小隐孢子虫激活的巨噬细胞产生氧化爆发，但对驻留巨噬细胞几乎没有活性。小鼠巨噬细胞通常对PAF-乙酰醚相当不敏感。另一方面，前列腺素（PG）E2是巨噬细胞氧化爆发的有效抑制剂，不过其活性也取决于巨噬细胞的来源和所用的刺激物。几种脂氧化酶抑制剂可抑制小鼠腹腔巨噬细胞的氧化爆发，而其他作者则报道了脂氧化酶产物对不同巨噬细胞群体的刺激作用。脂氧化酶和环氧化酶产物对巨噬细胞氧化爆发的不同作用，体现在花生四烯酸对酵母聚糖诱导的小鼠驻留腹腔细胞反应的影响上：先是增强，随后是长期抑制，后者对吲哚美辛敏感。虽然PAF-乙酰醚可能是体内巨噬细胞氧化爆发的重要启动因子，但花生四烯酸通过一种“跷跷板机制”调节反应，脂氧化酶产物起刺激作用，环氧化酶产物（主要是PGE2）起抑制作用。
