Watanabe K, Tanaka H, Tamaru N, Yoshida M
2nd Department of Medicine, School of Medicine, Fukuoka University, Japan.
Prostaglandins Leukot Essent Fatty Acids. 1993 Sep;49(3):675-81. doi: 10.1016/0952-3278(93)90076-9.
We investigated the effect of blood mononuclear cell-conditioned medium on prostacyclin (PGI2) production by human umbilical vein endothelial cells in culture (HUVEC), and compared the potency of the conditioned medium in PGI2 production with that of various cytokines and lipopolysaccharide (LPS). HUVEC which had been preincubated with LPS, interleukin-1 alpha (IL-1 alpha), IL-1 beta, tumor necrosis factor (TNF alpha), or interferon-gamma (IFN-gamma) produced more PGI2 than control cells in response to thrombin. However, the HUVEC preincubated with the conditioned medium made with mononuclear cells with or without LPS (LPS-Mo-CM, Mo-CM) produced more PGI2 than those preincubated with LPS, IL-1 alpha, IL-1 beta, TNF alpha, or IFN-gamma. Although the concentrations or IL-1 beta and TNF alpha in the post-culture medium of HUVEC treated with LPS-Mo-CM were much higher than those with Mo-CM, LPS-Mo-CM which was made with 13,000/ml of mononuclear cells and 1 microgram/ml of LPS did not significantly augment the subsequent PGI2 production by HUVEC as compared with Mo-CM made with the same numbers of mononuclear cells. PGI2 production by Mo-CM-treated HUVEC still exceeded that of control cells, even when an excess amount of antibody to TNF alpha and/or IL-1 alpha was added to the Mo-CM. It is possible that Mo-CM contains unknown cytokines besides IL-1 and TNF which stimulate the HUVEC to produce PGI2.
我们研究了血液单核细胞条件培养基对培养的人脐静脉内皮细胞（HUVEC）前列环素（PGI2）生成的影响，并将该条件培养基在PGI2生成方面的效力与各种细胞因子和脂多糖（LPS）的效力进行了比较。预先用LPS、白细胞介素-1α（IL-1α）、IL-1β、肿瘤坏死因子（TNFα）或干扰素-γ（IFN-γ）预孵育的HUVEC，在对凝血酶的反应中比对照细胞产生更多的PGI2。然而，用含或不含LPS的单核细胞制备的条件培养基（LPS-Mo-CM、Mo-CM）预孵育的HUVEC比用LPS、IL-1α、IL-1β、TNFα或IFN-γ预孵育的细胞产生更多的PGI2。尽管用LPS-Mo-CM处理的HUVEC培养后培养基中IL-1β和TNFα的浓度远高于用Mo-CM处理的，但用13000/ml单核细胞和1μg/ml LPS制备的LPS-Mo-CM与用相同数量单核细胞制备的Mo-CM相比，并未显著增加随后HUVEC的PGI2生成。即使向Mo-CM中加入过量的抗TNFα和/或抗IL-1α抗体，用Mo-CM处理的HUVEC的PGI2生成仍超过对照细胞。除了IL-1和TNF之外，Mo-CM可能还含有未知的细胞因子，这些因子刺激HUVEC产生PGI2。
