Kunkel S L, Wiggins R C, Chensue S W, Larrick J
Biochem Biophys Res Commun. 1986 May 29;137(1):404-10. doi: 10.1016/0006-291x(86)91224-6.
We have studied the role of prostaglandin E2 on the modulation of tumor necrosis factor by immunologically elicited and lipopolysaccharide treated murine macrophages. Indomethacin, a potent inhibitor of prostaglandin E2 production, caused a dose dependent augmentation of lipopolysaccharide induced tumor necrosis factor production (2-3 fold at 10(-7) molar). Tumor necrosis factor was released into the extracellular environment and no activity was found to be associated with membrane or cytosolic fractions. Prostaglandin E2 added to the lipopolysaccharide treated cultures suppressed tumor necrosis factor in a dose dependent manner. In these studies, 10(-7) molar PGE2 reduced tumor necrosis factor production to basal levels. These data suggest that PGE2 may be a potent autoregulatory factor that dramatically influences tumor necrosis factor production.
我们研究了前列腺素E2在免疫诱导和脂多糖处理的小鼠巨噬细胞对肿瘤坏死因子调节中的作用。吲哚美辛是前列腺素E2产生的强效抑制剂，它导致脂多糖诱导的肿瘤坏死因子产生呈剂量依赖性增加（10^-7摩尔时增加2至3倍）。肿瘤坏死因子释放到细胞外环境中，未发现与膜或胞质部分相关的活性。添加到脂多糖处理培养物中的前列腺素E2以剂量依赖性方式抑制肿瘤坏死因子。在这些研究中，10^-7摩尔的前列腺素E2将肿瘤坏死因子产生降低到基础水平。这些数据表明，前列腺素E2可能是一种强效的自调节因子，可显著影响肿瘤坏死因子的产生。
