Reduction of Complement Levels in Mice Infected with Trypanosoma cruzi

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Abstract
Complement (C) levels in 2 strains of mice that differ in susceptibility to T. cruzi were monitored during the course of infection. C3H (He) mice, which are highly susceptible to the parasite, exhibited a progressive decrease in C and died on about day 24 with approximately 43% of the normal level of C. C57BL/6 mice, which are more resistant and often survive experimental infections, underwent a reduction of C to approximately 15% of normal by day 30, a level that persisted until the experiment was terminated on day 45. Intact culture-form trypanosomes (live or formalin-treated), crude sonicates of the parasite or supernatants from cultured trypanosomes could decomplement normal serum by 30-70%. Selective chelation of Mg2+ and/or Ca2+ suggested that viable trypanosomes and trypanosome culture supernatants activate C, primary via the classical pathway. Collateral studies explored the relationship between the hypocomplementemic state and T. cruzi-induced immunosuppression. Transfer of serum (suppressive for humoral responses) from infected, syngeneic mice into normal recipients did not result in a significant reduction in C levels. The significance of lowered C levels during experimental Chagas'' disease is unclear. Hypocomplementemia apparently does not play a direct role in host susceptibility or the expression of parasite-induced immunosuppression.