Inhibition of macrophage-Trypanosoma cruzi interaction by concanavalin A and differential binding of bloodstream and culture forms to the macrophage surface.

The initial interaction between the surfaces of mouse peritoneal macrophages and Trypanosoma cruzi was examined using bloodstream (trypomastigote) and culture (epimastigote) forms of a predominantly reticulotropic strain of the parasite. Pretreatment with Con A resulted in a marked inhibition of macrophage binding of both forms of the parasite. Con A inhibition of epimastigote binding persisted for at least 4 hr after exposure to Con A whereas the trypomastigote-binding ability of macrophages showed a significant spontaneous recovery (57-79%) after 1 hr whether or not the parasites were present in the cell cultures during that time. Binding of Con A to the macrophage was required for inhibition of parasite attachment since incubation of Con A-treated cells with alpha-methyl mannoside prevented the inhibitory phenomenon when either epimastigotes or trypomastigotes were used. This monosaccharide had an inhibitory effect of its own which was not as marked as that produced by Con A and affected epimastigote but not trypomastigote binding to the phagocytic cells, thus representing an additional difference in the modes of interaction of these forms of the parasite with the macrophage surface. Furthermore, inhibition of either trypomastigote or epimastigote binding to macrophages was not caused by succinyl-Con A (which consists of two monomeric Con A subunits whereas Con A has four) unless the succinyl-Con A-treated macrophages were further incubated with anti-Con A antibodies. This observation suggests the importance of either molecular size or crosslinking of Con A subunits with consequent membrane rearrangement in causing the inhibitory phenomenon. The antibody preparation had no effect on macrophage binding of T. cruzi when tested by itself. These results highlight distinct characteristics of the binding of two forms of T. cruzi differing in their infective capacity to the surface of a host cell.