Tarleton R L
Department of Zoology, University of Georgia, Athens 30602.
Clin Exp Immunol. 1988 Aug;73(2):186-90.
Mice infected with the protozoan parasite Trypanosoma cruzi are primed for the production of tumour necrosis factor/cachectin. Active infection is not required for stimulation of TNF production as formalin-fixed, but not heat-killed, parasites can act as a priming stimulus. Both epimastigote and trypomastigote stages of the parasite can prime for TNF production but on a per cell basis, trypomastigotes are more potent stimulators than epimastigotes and live parasites prime more efficiently than killed preparations. Although the priming effect of epimastigotes and trypomastigotes is dose-dependent when assayed 10 days after parasite injection, parasitemia levels in the infected mice do not correlate with the level of TNF production. Spleen cells from infected mice are also primed for the production in vitro of TNF in response to LPS or T. cruzi. These results suggest that TNF may be constitutively produced in vivo and that the priming for TNF production, or the production itself, may be regulated during the course of the infection in mice.
感染原生动物寄生虫克氏锥虫的小鼠会启动肿瘤坏死因子/恶病质素的产生。刺激肿瘤坏死因子的产生并不需要活跃感染，因为经福尔马林固定而非热灭活的寄生虫可作为启动刺激物。寄生虫的前鞭毛体和锥鞭毛体阶段均可启动肿瘤坏死因子的产生，但按每个细胞计算，锥鞭毛体比前鞭毛体是更有效的刺激物，活寄生虫比灭活制剂更有效地启动。尽管在注射寄生虫10天后进行检测时，前鞭毛体和锥鞭毛体的启动效应呈剂量依赖性，但感染小鼠的寄生虫血症水平与肿瘤坏死因子的产生水平并无关联。来自感染小鼠的脾细胞也会启动，以便在体外对脂多糖或克氏锥虫产生肿瘤坏死因子。这些结果表明，肿瘤坏死因子可能在体内持续产生，并且在小鼠感染过程中，肿瘤坏死因子产生的启动或其产生本身可能受到调节。
