Interaction between cytochalasin B-treated malarial parasites and erythrocytes. Attachment and junction formation.
We have previously demonstrated that invasion of erythrocytes (RBCs) by malaria merozoites follows a sequence: recognition and attachment in an apical orientation associated with widespread deformation of the RBC, junction formation, movement of the junction around the merozoite that brings the merozoite into the invaginated RBC membrane, and sealing of the membrane. In the present paper, we describe a method for blocking invasion at an early stage in the sequence. Cytochalasin-treated merozoites attach specifically to host RBCs, most frequently by the apical region that contains specialized organelles (rhoptries) associated with invasion. The parasite then forms a junction between the apical region and the RBC. Cytochalasin blocks movement of this junction, a later step in invasion. Cytochalasin-treated (Plasmodium knowlesi) merozoites attach to Duffy-negative human RBCs, although these RBCs are resistant to invasion by the parasite. The attachment with these RBCs, however, differs from susceptible RBCs in that there is no junction formation. Therefore the Duffy associated antigen appears to be involved in junction formation, not initial attachment.
D000818:Animals; D001789:Blood Group Antigens; D002448:Cell Adhesion; D003571:Cytochalasin B / Q000494:pharmacology*; D004375:Duffy Blood-Group System; D004912:Erythrocytes / Q000469:parasitology* / Q000648:ultrastructure; D000882:Haplorhini; D006801:Humans; D007365:Intercellular Junctions / Q000648:ultrastructure; D008253:Macaca mulatta; D010961:Plasmodium / Q000187:drug effects* / Q000648:ultrastructure; D013696:Temperature
D001789:Blood Group Antigens; D004375:Duffy Blood-Group System; D003571:Cytochalasin B