Sayles P C, Cooley A J, Wassom D L
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison 53706.
Am J Trop Med Hyg. 1991 Jan;44(1):42-8. doi: 10.4269/ajtmh.1991.44.42.
The role of the spleen in resistance to infections with nonlethal Plasmodium yoelii 17x is dependent upon the genotype of the host. Thus, DBA/2 (D2) mice infected with P. yoelii 17x were not adversely affected by removal of the spleen, while splenectomized C57BL/6 (B6) or Balb/c mice failed to resolve their infections and eventually died. The levels of parasitemia were lower in splenectomized mice compared to intact controls; however, splenectomized mice became as anemic as did spleen-intact controls. Splenectomy resulted in the appearance of large aggregates of mononuclear cells in the livers of infected mice and also altered the liver/body weight ratios. These results indicate that D2 mice have a spleen-independent mechanism of clearing parasites which is lacking in B6 and Balb/c mice.
脾脏在抵抗非致死性约氏疟原虫17x感染中的作用取决于宿主的基因型。因此,感染约氏疟原虫17x的DBA/2(D2)小鼠切除脾脏后并未受到不利影响,而脾切除的C57BL/6(B6)或Balb/c小鼠无法清除感染,最终死亡。与完整对照组相比,脾切除小鼠的寄生虫血症水平较低;然而,脾切除小鼠与脾脏完整的对照组一样出现贫血。脾切除术导致感染小鼠肝脏中出现大量单核细胞聚集,并且改变了肝脏/体重比。这些结果表明,D2小鼠具有与脾脏无关的清除寄生虫机制,而B6和Balb/c小鼠缺乏这种机制。