Experimental Chagas' disease in complement-deficient mice and guinea pigs.
The course of infection with trypomastigotes of Trypanosoma cruzi (House 510 strain) in mice and guinea pigs with genetic complement deficiencies was compared with that in normocomplementemic animals. Parasitemias in a mouse strain (B10.D2/old) genetically deficient in C5 and therefore unable to sustain lysis were similar to or lower than in a congenic normocomplementemic strain (B10.D2/new). The levels of C3 measured immunochemically were generally unaffected. There were no significant differences in mortality rates. These results indicate that, in mice, complement-mediated lysis does not play a significant role in the control of T. cruzi (House 510) infections. Studies were also performed in normocomplementemic guinea pigs and in guinea pigs genetically deficient in the fourth component of complement and thus unable to support functions mediated by the classical pathway of complement activation. No significant differences were noted between the two strains in the course of infection, persistence of subpatent infection, or rate of mortality, indicating that if the classical complement pathway plays a role in resistance to T. cruzi (House 510) in guinea pigs, this role must be a small one.
D000818:Animals; D014355:Chagas Disease / Q000276:immunology*; D003181:Complement C4 / Q000235:genetics*; D003182:Complement C5 / Q000235:genetics*; D006168:Guinea Pigs / Q000235:genetics*; D008297:Male; D051379:Mice / Q000235:genetics*; D009132:Muscles / Q000473:pathology; D009206:Myocardium / Q000473:pathology
D003181:Complement C4; D003182:Complement C5