Boraschi D, Censini S, Bartalini M, Tagliabue A
J Immunol. 1985 Jul;135(1):502-5.
Mouse resident peritoneal M phi release AAA and metabolize it into cyclooxygenase- and lipoxygenase-derived eicosanoids, when triggered in vitro with different stimuli. Pretreatment of M phi with nonimmune IFN-alpha and IFN-beta dramatically decreased AA liberation from M phi phospholipids and eicosanoid formation after stimulation of M phi with Zy, A23187, or PMA. M phi exposed to immune IFN-gamma also showed a substantial impairment of both AA liberation and eicosanoid production upon exposure to Zy. However, AA and eicosanoid release was increased by IFN-gamma, rather than depressed, in PMA-triggered M phi. In addition, IFN-gamma showed differential effects on M phi stimulated with A23187. In fact, it inhibited AA release as well as formation of lipoxygenase-derived LTC4, but it highly increased the release of the cyclooxygenase products PGE2 and 6-keto PGF1 alpha. The ability of IFN-gamma to differentially modulate AA metabolism of M phi, depending on the nature of the triggering agent, sets forth the high specificity of the regulatory capacity of this molecule. This is at variance with the down regulation of AA metabolism that is generally observed with nonimmune IFN.
当在体外受到不同刺激时，小鼠腹腔驻留巨噬细胞会释放花生四烯酸（AAA）并将其代谢为环氧化酶和脂氧化酶衍生的类花生酸。用非免疫性干扰素-α和干扰素-β预处理巨噬细胞，在用酵母聚糖（Zy）、A23187或佛波酯（PMA）刺激巨噬细胞后，可显著降低巨噬细胞磷脂中花生四烯酸的释放和类花生酸的形成。暴露于免疫性干扰素-γ的巨噬细胞在接触酵母聚糖后，花生四烯酸的释放和类花生酸的产生也出现明显受损。然而，在PMA触发的巨噬细胞中，干扰素-γ会增加而非降低花生四烯酸和类花生酸的释放。此外，干扰素-γ对用A23187刺激的巨噬细胞表现出不同的作用。实际上，它抑制花生四烯酸的释放以及脂氧化酶衍生的白三烯C4（LTC4）的形成，但却显著增加环氧化酶产物前列腺素E2（PGE2）和6-酮前列腺素F1α（6-keto PGF1α）的释放。干扰素-γ根据触发剂的性质对巨噬细胞花生四烯酸代谢进行差异调节的能力，体现了该分子调节能力的高度特异性。这与非免疫性干扰素通常观察到的花生四烯酸代谢下调情况不同。
