The in vitro interaction of Trypanosoma cruzi bloodstream forms and mouse peritoneal macrophages.
The uptake and further development of bloodstream forms from T. cruzi Y and CL strains in mouse peritoneal macrophages have been investigated. Parasites from the Y strain (which present predominance of slender forms) are 20 to 30-fold more infective to macrophages than those from CL strain in which stout forms highly predominate. A complete amastigote-trypomastigote cycle is observed in normal or thioglycollate-induced macrophages infected with parasites from both strains.--Opsonization significantly increases the uptake by normal macrophages of parasites from both strains. The fate of the opsonizated parasites is, however, different: the Y trypomastigotes present a normal cycle which culminates with the release of newly formed trypomastigotes whereas CL parasites are extensively destroyed by normal macrophages.--The differences in the uptake and fate displayed by both T. cruzi populations are not well understood. They are apparently related to parasite membrane components or macrophage receptors differences, which are probably influencing endocytosis and the further intracellular development of the parasites.
D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D007106:Immune Sera / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000469:parasitology*; D051379:Mice; D008811:Mice, Inbred DBA; D009895:Opsonin Proteins; D013864:Thioglycolates / Q000494:pharmacology; D014349:Trypanosoma cruzi / Q000187:drug effects / Q000472:pathogenicity* / Q000528:radiation effects
D007106:Immune Sera; D009895:Opsonin Proteins; D013864:Thioglycolates