Premium
Acute virulent infection with Plasmodium chabaudi does not impair the generation of a protective immune response
Author(s) -
FALANGA PIERRE BARTHÉLÉMY,
SILVA LUIZ PEREIRA DA
Publication year - 1989
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1989.tb00924.x
Subject(s) - plasmodium chabaudi , immune system , biology , immunology , plasmodium yoelii , immunity , parasitemia , virulence , red blood cell , malaria , virology , plasmodium falciparum , gene , biochemistry
Summary We have investigated whether a protective immune response occurred in mice infected with a virulent cloned strain of Plasmodium chabaudi. Animals inoculated intravenously with 10′ parasitized erythrocytes (PE) showed an exponentially increasing parasitemia and died by day 6 of the infection, presenting a pronounced anaemia. Smaller inocula produced a longer pre–patent period but did not change the lethal course of infection, since mice injected with 100 parasites died on day 12. When anaemia was compensated for by red blood cell (RBC) transfusion, infected mice recovered and thereafter exhibited a strong immunity, comparable to that of mice immunized by a drug–controlled infection. The immune response was P. chabaudi specific, as the mice were fully susceptible to a challenge by P. yoelii. Three transfusions of 5 times 10′ RBC per mouse at 2–day intervals were necessary before all the animals were able to control the infection. Transfusion of a larger number of RBC resulted in a lower anaemia and a delay in reticulocytaemia but, paradoxically, the expression of the immune response was delayed. Three transfusions of 1–2 times 10 10 RBC enabled three out of eight mice to survive the infection, while six transfusions enabled all the mice to survive. The data suggest that parasitized immature RBC could play an important role in triggering the protective immune response.