犬バベシア感染にともなう赤血球膜の酸化傷害と貧血

贫血是吉氏巴氏杆菌感染犬的主要临床表现。感染犬血清中抗红细胞ELISA水平显著升高。为了阐明抗红细胞IgG抗体在吉氏B.gibsoni感染时贫血中的作用，建立了一种简单的红细胞表面结合IgG定量方法，并应用于感染犬和健康犬的结合IgG定量。临床感染犬的红细胞表面结合IgG值显著高于亚临床感染犬和健康犬，且升高水平与Coombs试验结果一致。在实验接种寄生虫红细胞之前和之后的狗的血清抗-RBC m抗体与自体或非自体RBC m的细胞骨架和跨膜结构（带3）蛋白反应。从吉氏B. gibsoni感染犬的红细胞中洗脱的抗-RBC m抗体与自身和非自身RBC m的条带3和4.2反应。抗-RBC m和用苯肼或神经氨酸酶处理的RBC表面，但不与未处理的处理RBC表面。基于此结果，认为B. gibsoni感染的狗的血清中的抗细胞骨架蛋白抗体附着于天然RBC m，此外，自由基诱导的红细胞氧化应激和红细胞糖蛋白中唾液酸的去除被认为是抗-吉氏B. gibsoni感染的狗的血清中的跨膜蛋白抗体与RBC结合。这些结果对阐明吉氏B.gibsoni感染后红细胞结合IgG值显著升高和贫血的机制具有重要意义。

Anemia is the primary clinical finding manifested by Babesia gibsoni-infected dogs. Significant elevated anti-erythrocyte ELISA levels were demonstrated in sera of infected dogs. To clarify the involvement of anti-erythrocyte IgG antibody in anemia during B.gibsoni infection, a simple method to quantify erythrocyte surface-bound IgG was established and applied to quantification of bound IgG in infected and healthy dogs. Erythrocyte surface-bound IgG value was shown to elevate significantly in clinical infected dogs compared to that of subclinically infected and healthy dogs, moreover the increased level was consistent with Coombs'test results. Serum anti-RBCm antibodies of the dogs before and after the experimental inoculation with parasitized erythrocytes reacted with cytoskeletal and transmembrane structural (band 3) proteins of either self or non-self RBCm. Anti-RBCm antibodies eluted from erythrocytes of B.gibsoni-infected dogs reacted with band 3 and 4.2 of self and non-self RBCm. Anti-RBCm and the surface of RBC treated with phenylhydrazine or neuraminidase, but not to that of non-treated treated RBC.Based from this results, anti-cytoskeletal protein antibody in sera of B.gibsoni-infected dogs is considered to attach to native RBCm, and furthermore free radical-induced oxidative stress imposed on RBC and sialic acid removal from grycoproteins of RBC are considered necessary for anti-transmembrane protein antibody in sera of B.gibsoni-infected dogs to be bound to RBCs. These are important to elucidating the mechanism of the marked in crease in RBCs-bound IgG value and anemia in B.gibsoni infection.