Otsuka Yayoi, Yamasaki Masahiro, Yamato Osamu, Maede Yoshimitsu
Department of Veterinary Clinical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
J Vet Med Sci. 2002 Mar;64(3):221-6. doi: 10.1292/jvms.64.221.
The role of macrophages in the erythrocyte membrane oxidative damage and the pathogenesis of anemia in Babesia gibsoni-infected dogs with low parasitemia were investigated. Macrophages derived from peripheral blood monocytes (PBM) from B. gibsoni-infected dogs produced significantly higher chemiluminescent responses, indicating the release of reactive oxygen intermediates, than those from non-infected dogs when the cells were subjected to non-specific stimulation with phorbol 12-myristate 13-acetate (PMA) and opsonized zymosan (OZ), or infected dog erythrocyte membranes opsonized with infected dog serum. These results indicate that PBM of B. gibsoni-infected dogs with low parasitemia were highly activated compared to those of non-infected dogs. Furthermore, the membrane lipid peroxidation of normal dog erythrocytes incubated with PBM from B. gibsoni-infected dogs was significantly higher (p<0.05) than that of erythrocytes incubated with PBM from non-infected dogs when the PBM were stimulated with the opsonized membranes. These results suggest that the oxidative damage of erythrocytes observed in B. gibsoni-infected dogs with low parasitemia might be induced, in part, by reactive oxygen species released from the activated PBM. On the other hand, the present study also showed a significant increase (p<0.001) of IgG-bound erythrocytes in B. gibsoni-infected dogs compared with such erythrocytes in non-infected dogs. The increase of IgG-bound erythrocytes in infected dogs might reflect the increase of erythrocytes with oxidative damage induced by the infection with B. gibsoni. The results of the present study suggest that the increase of IgG-bound erythrocytes in the circulation of infected dogs induce a high degree of erythrocyte loss via immunological phagocytosis by activated macrophages, resulting in severe anemia in spite of low parasitemia.
研究了巨噬细胞在吉氏巴贝斯虫感染且虫血症水平低的犬红细胞膜氧化损伤及贫血发病机制中的作用。当用佛波酯12 -肉豆蔻酸酯13 -乙酸酯（PMA）和调理酵母聚糖（OZ）进行非特异性刺激，或用感染犬血清调理感染犬红细胞膜时，来自吉氏巴贝斯虫感染犬外周血单核细胞（PBM）的巨噬细胞产生的化学发光反应显著高于未感染犬的巨噬细胞，这表明活性氧中间体的释放。这些结果表明，与未感染犬相比，吉氏巴贝斯虫感染且虫血症水平低的犬的PBM被高度激活。此外，当用调理后的膜刺激PBM时，与用未感染犬的PBM孵育的红细胞相比，用吉氏巴贝斯虫感染犬的PBM孵育的正常犬红细胞的膜脂质过氧化显著更高（p<0.05）。这些结果表明，在吉氏巴贝斯虫感染且虫血症水平低的犬中观察到的红细胞氧化损伤可能部分是由活化的PBM释放的活性氧引起的。另一方面，本研究还表明，与未感染犬的此类红细胞相比，吉氏巴贝斯虫感染犬中IgG结合红细胞显著增加（p<0.001）。感染犬中IgG结合红细胞的增加可能反映了吉氏巴贝斯虫感染诱导的氧化损伤红细胞的增加。本研究结果表明，感染犬循环中IgG结合红细胞的增加通过活化巨噬细胞的免疫吞噬作用导致高度的红细胞损失，尽管虫血症水平低，但仍导致严重贫血。
