Involvement of Trichomonas vaginalis surface-associated glycoconjugates in the parasite/target cell interaction. A quantitative electron microscopy study.

Cytochemical labeling with gold particle-conjugated lectins in combination with transmission and scanning electron microscopy was used to localise specific sugar residues on the Trichomonas vaginalis cell surface. For investigation of the role played by the surface glycoconjugates of T. vaginalis in the process of parasite adhesion to the target cells, selected glycan moieties of parasite surface-bound molecules were removed by treatment with alpha-mannosidase and beta-N-acetylglucosaminidase. For observation of the parasite/epithelial cell interaction, human amnion membrane was employed as an in vitro model. Ultrastructure observations showed that T. vaginalis has distinct binding sites for concanavalin-A and wheat-germ agglutinin. This indicates the presence of mannose or mannose-like residues and N-acetyl-D-glucosamine-containing residues on the parasite membrane. The addition of inhibitory sugars to T. vaginalis incubation media diminished the subsequent labeling of the parasite cell coat with lectins. Enzyme treatment caused a significant reduction in the number of sugar residues on the cell surface of the parasite. The majority of the viable, motile, enzyme-treated T. vaginalis cells incubated with amnion membrane were incapable of adhering to the target cells. It was concluded that sugar residues, in particular alpha-D-mannose and N-acetyl-glucosamine, present in the parasite glycocalyx are involved in the process of T. vaginalis attachment to the host's epithelial cells. Removal of the T. vaginalis cell-surface sugars prevented the attachment to and damage of the epithelial cells.

An electron microscope study of the interaction between Trichomonas vaginalis and epithelial cells of the human amnion membrane.

The mechanism of cytopathogenicity of Trichomonas vaginalis is not well established. Adhesion of T. vaginalis to human epithelial cells is considered a prerequisite for parasitic infection and its pathogenic effect. To investigate cytopathological changes in the host caused by T. vaginalis infection, human amnion membrane was used as an in vitro model. T. vaginalis strain WAA38 from axenic culture was allowed to interact with the epithelial layer of the human amnion membrane for 6 and 9 h. Structural changes resulting from the interaction between parasite and host cells were studied with transmission (TEM) and scanning (SEM) electron microscopy. Analysis of the electron microscope data showed that T. vaginalis established contact with the host cells as early as after 6 h of incubation; however, a close attachment of parasites to the epithelial cells occurred only after 9 h. Amoeboid T. vaginalis formed numerous cytoplasmic extensions and adhered to the epithelial cells mostly through the portions of their body opposite the undulating membrane. A dense network of microfilaments was seen at the site of contact between T. vaginalis and epithelial cells. Damaged and desquamated epithelial cells were seen with TEM and SEM only in the areas where parasites were in direct contact with target cells.