Role of surface N-acetylglucosamine residues on host cell infection by Trypanosoma cruzi.
We studied the role of surface GlcNAc residues on the surface of invasive (mouse-blood and insect-derived trypomastigotes) and non-invasive amastigote forms of Trypanosoma cruzi on parasite association with (i.e., surface binding plus internalization) macrophages and heart myoblasts. Removal of GlcNAc from the three forms of the parasite with beta-N-acetylglucosaminidase markedly increased the number of organisms per 100 cells and caused the organisms to associate with a greater percentage of host cells. N-Acetylglucosaminidase did not produce this effect after heat-inactivation and a substrate of the enzyme, N,N'-diacetylchitobiose, reduced it when it was present during the enzymatic treatment. The N-acetylglucosaminidase effect on T. cruzi was reversible after 2.5 h. When macrophages or myoblasts were treated with N-acetylglucosaminidase, their capacities to associate with blood or insect-derived trypomastigotes was reduced. Since removal of GlcNAc residues from the parasite surface increased their association with the host cells, GlcNAc would appear to interfere with the association process. On the other hand, GlcNAc residues on the host cell appear to favor the association.
D000117:Acetylglucosamine / Q000502:physiology*; D000118:Acetylglucosaminidase / Q000494:pharmacology; D000818:Animals; D001202:Ascitic Fluid; D002462:Cell Membrane / Q000187:drug effects / Q000469:parasitology*; D002478:Cells, Cultured; D005944:Glucosamine / Q000031:analogs & derivatives*; D006321:Heart / Q000469:parasitology; D008264:Macrophages / Q000469:parasitology; D051379:Mice; D008808:Mice, Inbred CBA; D051381:Rats; D014349:Trypanosoma cruzi / Q000187:drug effects / Q000254:growth & development / Q000502:physiology*
D000118:Acetylglucosaminidase; D005944:Glucosamine; D000117:Acetylglucosamine