Taffet S M, Eurell T E, Russell S W
Prostaglandins. 1982 Dec;24(6):763-74. doi: 10.1016/0090-6980(82)90057-0.
Mouse resident peritoneal macrophages stimulated in vitro by purified bacterial lipopolysaccharide (LPS) produced both prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2), the latter detected as its stable metabolite, 6-keto PGF1 alpha. Maximum production, induced in each case by 1 ng/ml purified LPS, was in the range of 10(-7)M for PGI2 and 3 x 10(-8)M for PGE2. A quantitatively similar increase in intracellular levels of macrophage cyclic AMP (measured on a whole cell basis), with a similar duration of effect, was stimulated by PGE2 and PGI2; however, only PGE2 had a negative regulatory effect on macrophage activation for tumor cell killing. These data confirm that more than a whole cell increase in the concentration of cyclic AMP is needed to shut off nonspecific tumor cell killing mediated by LPS-activated resident peritoneal macrophages.
经纯化的细菌脂多糖（LPS）体外刺激的小鼠腹腔常驻巨噬细胞可产生前列腺素E2（PGE2）和前列腺素I2（PGI2），后者通过其稳定代谢产物6-酮-前列腺素F1α检测。每种情况下，由1 ng/ml纯化LPS诱导的最大产量，PGI2为10^(-7)M，PGE2为3×10^(-8)M。PGE2和PGI2刺激巨噬细胞环磷酸腺苷（以全细胞为基础测量）的细胞内水平有类似的定量增加，且作用持续时间相似；然而，只有PGE2对巨噬细胞杀伤肿瘤细胞的激活具有负调节作用。这些数据证实，要关闭由LPS激活的腹腔常驻巨噬细胞介导的非特异性肿瘤细胞杀伤，需要的不仅仅是环磷酸腺苷浓度在全细胞水平上的增加。
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