Sanin A V, Khorobrykh V V
Biull Eksp Biol Med. 1982 Mar;93(3):72-4.
M. arthritidis injected into B6AF1 hybrid mice 24 hours after 5-FU administration was shown to promote rapid erythropoiesis recovery in the spleen as measured by 59Fe incorporation M. arthritidis injected 4 hours after the drug or 4 hours before it was less effective. When inoculated 24 hours before 5-FU, M. arthritidis caused retardation of erythropoiesis recovery. The splenic 59Fe incorporation rise in all the cases paralleled the increase in cellularity with an overshoot at day 10-15 after 5-FU administration. In the femoral bone marrow, 59Fe incorporation was decreased in the mycoplasma-infected mice compared with the mice which received the drug alone. The results indicate that M. arthritidis is likely to trigger the resting hemopoietic precursor cells into the proliferative cycle. Another possible mechanism of M. arthritidis action might involve the increased migration of erythroid cell from the bone marrow to the spleen. The mode of M. arthritidis action on hemopoiesis in mice is different from that of bacterial endotoxin and erythropoietin.
在给予5-氟尿嘧啶(5-FU)24小时后,向B6AF1杂交小鼠注射关节炎支原体,结果显示,通过59Fe掺入量测定,其可促进脾脏中红细胞生成的快速恢复。在给药后4小时或给药前4小时注射关节炎支原体,效果较差。在5-FU给药前24小时接种关节炎支原体,会导致红细胞生成恢复延迟。在所有情况下,脾脏中59Fe掺入量的增加与细胞数量的增加平行,在5-FU给药后第10 - 15天出现超调。在股骨骨髓中,与仅接受药物的小鼠相比,支原体感染小鼠的59Fe掺入量降低。结果表明,关节炎支原体可能会促使静止的造血前体细胞进入增殖周期。关节炎支原体作用的另一种可能机制可能涉及红系细胞从骨髓向脾脏迁移的增加。关节炎支原体对小鼠造血作用的方式不同于细菌内毒素和促红细胞生成素。