THE ROLE OF MACROPHAGES ON THE PATHOGENESIS OF BABESIOSIS

本研究旨在探讨吉氏巴氏巴氏杆菌感染红细胞氧化过程的机制，特别是巨噬细胞在此过程中的作用。结果表明，B. gibsoni值显著高于对照组。当B.结果表明，红细胞超氧化物歧化酶（SOD）的产生量高于对照组，红细胞超氧化物歧化酶（SOD）的产生量高于对照组。感染狗的巨噬细胞产生的超氧化物的量比那些未感染的狗，当细胞受到感染的狗红细胞膜与感染的狗血清调理。感染犬红细胞与巨噬细胞共孵育后，其膜脂质过氧化水平明显高于未感染犬。提示B.具有低寄生虫血症的Gibsoni感染的狗可能是由活化的巨噬细胞释放的超氧化物诱导的。

The present study was carried out to elucidate the mechanisms underlying the oxidative process in Babesia gibsoni-infected erythrocyte(RBC), especially the role of macrophage in the process. As the results, the generation of superoxide anion and the oxidative damage in RBC of dogs infected with B. gibsoni was significantly higher than those in control RBC. When B. gibsoni was cultured together with RBC, superoxide generation of RBC was higher in the parasitized culture than the control culture. The macrophages of infected dogs produced a higher amount of superoxide than those of non-infected dogs, when the cells were subjected to infected dog RBC membrane opsonized with infected dog serum. The membrane lipid peroxidati of RBC incubated with macrophages from infected dogs was higher than that from non-infected dogs. These results suggest that the oxidative damage of RBC in B. gibsoni-infected dogs with a low parasitemia might be induced by superoxide released from the activated macrophages.