Complement in experimental Trypanosoma lewisi infection of rats

Abstract

The role of complement [C] in host resistance to infection with T. lewisi was studied in normal, C4-deficient and C3-depleted rats. C levels were measured in normal rats throughout the course of infection. A drastic reduction of total C and C4 hemolytic activities occurred, and C3 levels measured immunochemically were decreased. Although total C and C4 levels were regularly reduced to < 10% of preinfection levels regardless of parasite numbers, the degree of C3 consumption correlated with the parasitemia. C3 levels varied from 100% of preinfection in rats with light infections to 35% in animals with heavy parasitemias. Recovery to normal levels followed trypanosome elimination from the peripheral blood. The infection had no significant effect on C6 hemolytic activity. Parasitemias and C3 levels in C4-deficient rats did not differ from those of normocomplementemic controls. Depletion of C3 and late-acting components by cobra venom factor during the reproductive or adult stages of infection did not alter the parasitemias. T. lewisi and immune serum caused C activation in vitro, which could be inhibited with ethylene glycol-bis-(.beta.-aminoethyl ether)N,N''-tetraacetic acid or EDTA. Although T. lewisi infections in rats result in activation of the classical C pathway with extensive consumption of the early-acting components and a low degree of activation of the alternative pathway, C does not appear to play a major role in the control and termination of the infection.