Acquired macrophage resistance to in vitro infection with Leishmania.
An important feature of pathogenesis in leishmaniasis is the ability of the intracellular amastigote to gain entry into host mononuclear phagocytes and subsequently replicate. Resident peritoneal macrophages freshly harvested from Leishmania tropica-infected C57B1/6 mice and uninfected controls were therefore compared for their ability to ingest L tropica amastigotes in vitro. Macrophages from infected mice had a strikingly reduced ability to ingest parasites, but they ingested latex beads and IgG-sensitized erythrocytes as well as or more than control macrophages. Preincubation of these macrophages for 24 hr restored the degree of parasite ingestion to control levels. This alteration in macrophage function could be observed as early as two weeks of infection and persisted until spontaneous resolution of the infection occurred at about six weeks. The observations suggest that acquired defense in leishmaniasis may include a specific inhibition of amastigote uptake by host macrophages.
D000818:Animals; D001202:Ascitic Fluid; D002478:Cells, Cultured; D005260:Female; D006790:Host-Parasite Interactions; D007891:Leishmania / Q000502:physiology*; D007896:Leishmaniasis / Q000276:immunology / Q000469:parasitology*; D008264:Macrophages / Q000276:immunology / Q000469:parasitology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010587:Phagocytosis