Killing of Leishmania tropica amastigotes by factors in normal human serum.
Amastigotes of Leishmania tropica and L. donovani were incubated with fresh or heat-inactivated normal human serum. Viability was estimated by amastigote conversion to promastigote forms and by the ability of serum-treated amastigotes to infect human monocytes. L. tropica, a parasite that causes local skin infection, was killed by fresh but not by heat-inactivated serum. The serum cytotoxic effect on L. tropica was inhibited by EDTA but not by Mg-EGTA. C2-deficient serum killed normally; C6-deficient serum was ineffective. These data indicate that L. tropica is killed by the complement membrane attack complex, in a sequence of reactions initiated by components of the alternate pathway. In contrast, L. donovani, a parasite that causes systemic visceral leishmaniasis, was 10-fold less susceptible to the cytotoxic effects of normal serum. Thus, a profound difference exists in the susceptibility of amastigotes of two species of Leishmania to a defense mechanism present in human serum. Serum complement factors may play an important role in limiting L. tropica to the skin. The resistance of L. donovani to such factors may be the primary reason for its ability to escape from the site of inoculation and cause catastrophic, disseminated disease.
D000818:Animals; D001790:Blood Physiological Phenomena; D003170:Complement Pathway, Alternative; D003602:Cytotoxicity, Immunologic; D004306:Dose-Response Relationship, Immunologic; D006358:Hot Temperature; D006801:Humans; D007700:Kinetics; D007891:Leishmania / Q000254:growth & development* / Q000276:immunology / Q000502:physiology; D007896:Leishmaniasis / Q000276:immunology* / Q000469:parasitology; D007898:Leishmaniasis, Visceral / Q000276:immunology* / Q000469:parasitology; D051379:Mice; D008807:Mice, Inbred BALB C