Host cell invasion by Trypanosoma cruzi: role of cell surface galactose residues.
Alpha-galactosidase treatment of blood, insect and intracellular forms of T. cruzi enhanced their ability to associate with mouse peritoneal macrophages or rat heart myoblasts as evidenced by significant increases in both the percentage of infected cells and the number of parasites per cell. The magnitude of the enhancement was greater with invasive (blood and insect) than with noninvasive (intracellular) forms of the parasite. The enzyme effect was reversible, attaining total recovery in 2.5 hr. By contrast, when either host cell was pretreated with the enzyme, the extent of cell-parasite association was significantly reduced. These results indicate that galactose residues on T. cruzi and host cells modulate their association in opposite ways.
D000818:Animals; D001202:Ascitic Fluid; D002478:Cells, Cultured; D005690:Galactose / Q000502:physiology*; D006321:Heart / Q000469:parasitology*; D006790:Host-Parasite Interactions; D008264:Macrophages / Q000469:parasitology*; D051379:Mice; D008808:Mice, Inbred CBA; D051381:Rats; D014349:Trypanosoma cruzi / Q000187:drug effects / Q000502:physiology*; D000519:alpha-Galactosidase / Q000494:pharmacology
D000519:alpha-Galactosidase; D005690:Galactose