中国寄生虫学与寄生虫病杂志 ›› 1997, Vol. 15 ›› Issue (6): 335-339.

• 论著 • 上一篇    下一篇

IFN-γ激活巨噬细胞产生一氧化氮杀伤疟原虫的作用

牛宇欣1; 李慧珠2; 张海燕3; 王凤芸2   

  1. 1 首都医科大学细胞与遗传教研室; 2 首都医科大学寄生虫学教研室; 3 首都医科大学细胞学教研室
  • 收稿日期:1900-01-01 修回日期:1900-01-01 出版日期:1997-12-28 发布日期:1997-12-28

OLE OF NITRIC OXIDE PRODUCED BY IFN-γ-ACTIVATED MACROPHAGECSIN THE KILLING OF MALARIA PARASITE

Niu Yuxin1; L i Huizhu2; Zhang Haiyan3; Wang Fengyun2   

  1. 1 Departmentof Cytobiology and Genetics; Capital University of Medical Sciences; Beijing100054 2 Department of parasitology, Capital University of Medical Sciences, Beijing 1000543 Department of Cytobiology, Capital University of Medical Sciences, Beijing 100054
  • Received:1900-01-01 Revised:1900-01-01 Online:1997-12-28 Published:1997-12-28

摘要: 目的 :观察 IFN- γ激活的巨噬细胞 ( MΦ)合成的一氧化氮 ( NO)及其在疟疾保护性免疫中杀伤疟原虫的作用。方法 :体外分离培养小鼠腹腔 MΦ,与不同浓度的 γ干扰素 ( IFN- γ)共育 4 8h后 ,加入分离的寄生疟原虫的红细胞 ,观察激活的 MΦ NO产生水平及其对疟原虫的杀伤作用。结果 :IFN-γ能激活 MΦ产生 NO,其产生的量与IFN-γ的浓度有关 ;MΦ对疟原虫的杀伤作用与 NO的释放量呈显著相关关系 ( r=0 .898,n=13,P<0 .0 1) ;N-硝基 -
L -精氨酸 ( N- nitro-L- arginine,L- NNA)能抑制 NO合成 ,同时也降低 MΦ 的杀伤活性 ;感染约氏疟原虫的 BAL B/c小鼠注射 L- NNA,导致原虫血症上升 ,小鼠死亡率升高。结论 :IFN- γ激活 MΦ产生 NO可能是杀伤疟原虫的重要作用机制。

关键词: IFN-γ, 巨噬细胞, 一氧化氮, 约氏疟原虫, 原虫血症

Abstract: AIM:To explore the role of nitric oxide (NO) produced by IFN- γ- activated macrophages
in the killing of malaria parasite.METHODS:After the isolated murine peritonal macrophages were
inoculated with IFN- γ of different concentrations for48h, P.yoelii parasitized erytherocytes(PRBCs)
were added for another4h.For in vivo studies mice were infected ip with107 PRBCs,NO produced by IFN-
γ- activated- macrophages both in vitro and in vivo were measured and the cytotoxicity of macrophage
on Plasmodium yoelii parasites was examinded. RESULTS: A positive correlation was found between the cytotoxicity of macrophages and NO levels ( r= 0.898, P < 0.01). L-NNA, an inducible NO synthase (iN-OS) competitive inhibitor, could inhibit the production of NO by macrophages and reduced the cytotoxicity ofmacrophages cytotoxicity on P. yoelii. IFN- γ was found to protect BALB/c mice against P. yoelii infection in vivo, while in jection of L-NNA resulted in high level of parasitemia and increased mortality in infected mice. CONCLUSION: The plasmodicidal cytotoxicity could be attributed to the nitric oxide produced by the IFN -γ-activated macrophages.

Key words: Interferon- γ, macrophage s cytotoxicity, nitric oxide, Plasmodium yoelii, parasitemi