The role in vivo of C3 and the C3b receptor in babesial infection in the rat.

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Abstract
The critical role of complement (C3) and the C3b receptor in facilitating the in vivo development of parasitemia with Babesia rodhaini in rats is documented. Depletion of serum C3 to less than 5% of normal levels by treatment of rats with the C3 inactivator isolated from cobra venom markedly delays the onset of parasitemia. Treatment of rats with trypan blue, an inhibitor of the C3b receptor, delays the development of parasitemia. Conversely, treatment of rats with suramin, a drug that blocks the C3b inactivator, markedly accelerates the progression of parasitemia and, correspondingly, the mortality rate. These observations suggest that the in vivo production of C3b and its interaction with C3b receptors on red cells and/or on parasites is a critical feature in babesial injection of rats. In support of the concept that B. rodhaini organisms contain C3b receptors, we have shown in vitro that parasites will activate the alternate complement pathway, resulting in uptake of radiolabeled C3, and that this uptake is blocked in the presence of trypan blue. Before and during the development of parasitemia, red cells become Coombs-positive for C3, but not for IgG. Taken together, the data support the vital role of C3 activation products (presumably C3b) and the C3b receptor in the facilitation of babesial infection in the rat.