Ackermann M F, Mark R, Chakraborty P R, Morahan P S
J Leukoc Biol. 1986 Nov;40(5):549-59. doi: 10.1002/jlb.40.5.549.
Exposure of mice to diethylstilbestrol (DES) inhibited Propionibacterium acnes-induced antitumor activity in vivo against the B16F10 subcutaneous tumor. The inhibitory effect was associated with inhibition by DES of the characteristic P. acnes induced splenomegaly and changes in splenic and peritoneal macrophages (M phi) cell populations. The characteristic P. acnes induced reductions in M phi alkaline phosphodiesterase I (APD) ectoenzyme activity and in total RNA synthesis, proposed biochemical markers of tumoricidal M phi, were partially or completely reversed in DES-treated mice. As predicted from these in vivo and in vitro results, DES treatment significantly decreased P. acnes activation of M phi antitumor activity in vitro against B16F10 melanoma and Lewis lung carcinoma cells. These data suggest a macrophage activation defect may be involved in the reduced resistance that DES-treated animals exhibit to a variety of neoplastic and microbial challenges.
将小鼠暴露于己烯雌酚（DES）会抑制痤疮丙酸杆菌在体内对B16F10皮下肿瘤的抗肿瘤活性。这种抑制作用与DES对痤疮丙酸杆菌诱导的脾肿大以及脾和腹膜巨噬细胞（M phi）细胞群体变化的抑制有关。痤疮丙酸杆菌诱导的M phi碱性磷酸二酯酶I（APD）外切酶活性降低以及总RNA合成减少，这是具有杀肿瘤活性M phi的生化标志物，在DES处理的小鼠中部分或完全得到逆转。根据这些体内和体外结果预测，DES处理显著降低了痤疮丙酸杆菌在体外对B16F10黑色素瘤和Lewis肺癌细胞的M phi抗肿瘤活性的激活。这些数据表明，巨噬细胞激活缺陷可能与DES处理的动物对各种肿瘤和微生物挑战表现出的抵抗力降低有关。
