Dan K, Gomi S, Inokuchi K, Ogata K, Yamada T, Ohki I, Hasegawa S, Nomura T
Third Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
Acta Haematol. 1995;93(2-4):67-72. doi: 10.1159/000204114.
We studied the effects of interleukin-1 (IL-1) and tumor necrosis factor (TNF) on mouse megakaryocytopoiesis to evaluate the role of these cytokines in reactive thrombocytosis associated with inflammation. Injections of IL-1 or TNF to mice induced a significant increase in the megakaryocyte progenitor cell (CFU-Meg) count in the spleen. When IL-1 and TNF were injected simultaneously, the splenic CFU-Meg count was remarkably increased compared with mice injected with either IL-1 (p < 0.003) or TNF (p < 0.001) alone. On the other hand, neither IL-1 nor TNF showed any megakaryocyte-potentiating or -stimulating effects in vitro. In the sera obtained 4 h after administration of IL-1, TNF or both, high megakaryocyte potentiating activities were found. Furthermore, an extremely high level of IL-6 was detected in the serum after administration of both IL-1 and TNF. These results strongly suggest that IL-1 and TNF stimulate megakaryocytopoiesis indirectly via other cytokine(s) induced from accessory cells, and that increased levels of IL-1 and TNF play important roles in the development of reactive thrombocytosis caused by inflammation.
我们研究了白细胞介素-1（IL-1）和肿瘤坏死因子（TNF）对小鼠巨核细胞生成的影响，以评估这些细胞因子在与炎症相关的反应性血小板增多症中的作用。给小鼠注射IL-1或TNF可导致脾脏中巨核细胞祖细胞（CFU-Meg）数量显著增加。当同时注射IL-1和TNF时，与单独注射IL-1（p < 0.003）或TNF（p < 0.001）的小鼠相比，脾脏CFU-Meg数量显著增加。另一方面，IL-1和TNF在体外均未显示出任何巨核细胞增强或刺激作用。在给予IL-1、TNF或两者后4小时获得的血清中，发现了高巨核细胞增强活性。此外，在给予IL-1和TNF后，血清中检测到极高水平的IL-6。这些结果强烈表明，IL-1和TNF通过辅助细胞诱导的其他细胞因子间接刺激巨核细胞生成，并且IL-1和TNF水平的升高在由炎症引起的反应性血小板增多症的发展中起重要作用。
