This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Jarvinen, J A Articles by Dalmasso, A P Search for Related Content PubMed PubMed Citation Articles by Jarvinen, J A Articles by Dalmasso, A P

 Previous Article  |  Next Article 

Infect Immun. 1976 October; 14(4): 894-902

Complement in experimental Trypanosoma lewisi infection of rats.

ABSTRACT

The role of complement in host resistance to infection with Trypanosoma lewisi was studied in normal, C4-deficient, and C3-depleted rats. Complement levels were measured in normal rats throughout the course of infection. A drastic reduction of total complement and C4 hemolytic activities occurred, and C3 levels measured immunochemically were decreased. Although total complement and C4 levels were regularly reduced to less than 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. In addition, T. lewisi and immune serum caused complement activation in vitro, which could be inhibited with ethylene glycol-bis-(beta-aminoethyl ether)N,N'-tetraacetic acid or ethylenediaminetetraacetic acid. It is concluded that T. lewisi infection in rats result in activation of the classical complement pathway with extensive consumption of the early-acting components, as well as a low degree of activation of the alternative pathway. However, complement does not appear to play a major role in the control and termination of the infection.