Zor U, Ben-Dori R, Maoz I, Wallach D, Gurari-Rotman D
J Gen Virol. 1982 Dec;63(2):359-63. doi: 10.1099/0022-1317-63-2-359.
We have examined the relationship between induction of interferon (IFN) and prostaglandin E (PGE) production by poly(rI).poly(rC) in cultured human foreskin fibroblasts (FS11). Hydrocortisone and dexamethasone (2 . 5 x 10(-7) M), which are known inhibitors of PGE synthesis, significantly decreased the induction of both IFN and PGE in IFN-pretreated (primed) cells. Desoxycorticosterone, progesterone and estradiol were devoid of this activity. Hydrocortisone also blocked the induction of IFN by double-stranded RNA (dsRNA), cycloheximide and actinomycin D in FS11 cells. Arachidonic acid overcame the inhibitory effect of hydrocortisone on PGE production, but failed to restore IFN production in the presence of the steroid. Moreover, the prostaglandin synthetase inhibitors, indomethacin, aspirin and flufenamic acid, did not change IFN production by dsRNA in primed FS11 cells, although prostaglandin synthesis was abolished. Although the induction of IFN and PGE by poly(rI).poly(rC) might be consequences of the same initial event in the cell, the accumulation of PGE does not seem to have a regulatory effect on the synthesis of IFN in this system.
我们研究了在培养的人包皮成纤维细胞（FS11）中，聚肌苷酸-聚胞苷酸（poly(rI).poly(rC)）诱导干扰素（IFN）与前列腺素E（PGE）产生之间的关系。已知的PGE合成抑制剂氢化可的松和地塞米松（2.5×10⁻⁷ M），显著降低了IFN预处理（致敏）细胞中IFN和PGE的诱导水平。脱氧皮质酮、孕酮和雌二醇没有这种活性。氢化可的松还阻断了FS11细胞中双链RNA（dsRNA）、环己酰亚胺和放线菌素D对IFN的诱导。花生四烯酸克服了氢化可的松对PGE产生的抑制作用，但在存在类固醇的情况下未能恢复IFN的产生。此外，前列腺素合成酶抑制剂吲哚美辛、阿司匹林和氟芬那酸，虽然消除了前列腺素合成，但并未改变致敏的FS11细胞中dsRNA诱导的IFN产生。尽管poly(rI).poly(rC)诱导IFN和PGE可能是细胞中同一初始事件的结果，但在该系统中，PGE的积累似乎对IFN的合成没有调节作用。
