Abstract
Leishmaniasis is a typical parasite infection whose protective immunity depends on macrophage activation. Susceptibility to Leishmania donovani infection was compared in H (high antibody responder) and L (low antibody responder) mice from selection IV-A. H mice infected intravenously with 10(7) amastigotes of L. donovani were more susceptible to infection than their L counterparts. This higher susceptibility was characterized by a higher splenic and hepatic parasite burden. An increased splenic index was observed in both lines after sixty days of infection. This splenomegaly was caused, at least partially, by an increase in the number of splenic cells as determined by direct counts of cells from spleen. The results show that selection IV-A is susceptible to visceral leishmaniasis, with the H line being more susceptible than the L line.
Highlights
Leishmaniasis is a typical parasite infection whose protective immunity depends on macrophage activation
Considering that L. donovani is an intracellular parasite and that the macrophage function is altered in selection IV-A, the purpose of this study was to evaluate the susceptibility of H and L mice from selection IV-A to infection with L. donovani
Liver parasite counts on the first day showed no difference between H and L mice, with 138 LeishmanDonovan Units (LDU) being the mean count for both lines
Summary
Leishmaniasis is a typical parasite infection whose protective immunity depends on macrophage activation. Susceptibility to Leishmania donovani infection was compared in H (high antibody responder) and L (low antibody responder) mice from selection IV-A. Selection IV-A was derived from F2 interline segregants between HIV and LIV lines in response to SE9 This approach has permitted to establish that quantitative antibody production is a polygenic trait regulated by a group of about 10 independent loci[2 14]. Low antibody responses in Lmice have been attributed to higher catabolism of immunogens in the macrophages and consequent decreased antigen presentation by these cells. These macrophage catabolic differences have been previously demonstrated in selections I, II and IV-A16
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