Injury induced by Trypanosoma congolense adhesion to cell membranes.
Trypanosoma congolense binds to erythrocytes and the walls of the microvasculature. Experiments were conducted to determine if the attachment of T. congolense, alone or in combination with antitrypanosome antibody, was damaging to host cells. Bovine erythrocytes were labelled with 51Cr and incubated with T. congolense to promote adhesion. Plasma from the same donor as the red blood cells was added to the erythrocyte-trypanosome aggregates and the release of 51Cr measured. There was a two- to threefold increase in 51Cr release when trypanosomes were lysed by antibody-complement interaction following adhesion to the erythrocyte. The erythrocytes were not damaged by trypanosome binding in the absence of antibody or complement. A similar mechanism may operate in vivo because experiments demonstrated an increased vascular permeability of mesenteric vessels, a site of T. congolense attachment to the microcirculation. These results suggest that the adhesion of T. congolense to host cells, followed by an immune response to the parasite, may damage the infected host by "innocent bystander" mechanisms.
D000818:Animals; D000906:Antibodies; D000937:Antigen-Antibody Reactions; D002199:Capillary Permeability; D002417:Cattle; D003165:Complement System Proteins; D004910:Erythrocyte Membrane / Q000469:parasitology*; D004912:Erythrocytes / Q000469:parasitology*; D006461:Hemolysis; D008833:Microcirculation / Q000469:parasitology; D014345:Trypanosoma / Q000276:immunology / Q000502:physiology*; D014354:Trypanosomiasis, Bovine / Q000276:immunology / Q000469:parasitology*
D000906:Antibodies; D003165:Complement System Proteins