Inamura N, Nakahara K, Kuroda Y, Yamaguchi I, Aoki H, Kohsaka M
Exploratory Research Laboratories, Fujisawa Pharmaceutical Co. Ltd., Ibaraki, Japan.
Int J Immunopharmacol. 1988;10(5):547-54. doi: 10.1016/0192-0561(88)90072-0.
Nocardia rubra cell wall skeleton (N-CWS) was shown to augment interleukin 1 (IL-1) production from peritoneal resident and exudate macrophages in C3H/HeN mice. The mol. wt of the N-CWS-induced IL-1 product was about 17,000 daltons, which is a similar weight to that obtained by lipopolysaccharide stimulation. The stimulation of IL-1 production by N-CWS was seen as early as 8 h after the start of incubation and peak production was observed at 48 h. Profound effects were seen with 10 micrograms/ml or more of N-CWS. Experiments on the regulation of the N-CWS-augmented IL-1 production showed that prostaglandin E2 inhibited the augmentation, and indomethacin (cyclo-oxygenase inhibitor) further augmented it. Leukotriene B4 and AA861 (lipoxygenase inhibitor) had no effect. Our findings suggest that the previously reported adjuvant effect of N-CWS may, in part, be mediated via its ability to stimulate IL-1 production; and that such a stimulation may be blocked by prostaglandins.
已证明红色诺卡氏菌细胞壁骨架(N-CWS)可增强C3H/HeN小鼠腹腔常驻巨噬细胞和渗出巨噬细胞产生白细胞介素1(IL-1)的能力。N-CWS诱导产生的IL-1产物的分子量约为17,000道尔顿,这与脂多糖刺激所获得的分子量相似。N-CWS对IL-1产生的刺激最早在孵育开始后8小时出现,48小时时观察到产量峰值。10微克/毫升或更高浓度的N-CWS可产生显著效果。关于N-CWS增强IL-1产生的调节实验表明,前列腺素E2可抑制这种增强作用,而吲哚美辛(环氧化酶抑制剂)则可进一步增强其作用。白三烯B4和AA861(脂氧合酶抑制剂)没有作用。我们的研究结果表明,先前报道的N-CWS的佐剂作用可能部分是通过其刺激IL-1产生的能力介导的;并且这种刺激可能被前列腺素阻断。