immunology of infectious and parasitic diseases - XXXVII Congress ...

SERUM COMPONENTS AND MONONUCLEAR CELLS COOPERATE TO
RAPIDLY CONTROL AN AVIRULENT PROTOZOAN PARASITE
NICOLI DE BONA HECK 1 ; STEFANNY V. MORALES 1 ; ÁLVARO MENIN 1 ;
PATRÍCIA STOCO 2 ; DÉBORA LÜCKEMEYER 2 ; MÁRIO STEINDEL 2 ;
EDMUNDO C. GRISARD 2 ; ANDRÉ BAFICA 1 .
1 Laboratory of Immunobiology, MIP-UFSC; 2 Laboratory of Protozoology, MIP-
UFSC.
Introduction: Trypanosoma rangeli has been documented to be a non-virulent
protozoan parasite in mammalian hosts. However, information regarding T.
rangeli-host interactions during infection remains scarce.
Methods and Results: In this study, parasitemia as well as immune responses
of C57BL/6 mice i.p. injected with culture-derived T. rangeli trypomastigotes
(Choachí strain) were assessed. T. rangeli trypomastigotes were found in the
blood of infected mice as early as 1 day p.i., reaching a peak of parasitemia at 2
days p.i. Parasite clearance occurred by day 9 p.i. Surprisingly, histological
analysis of the liver revealed that this parasite elicited a robust inflammatory
infiltrate prominent in mononuclear cells that persisted up to 60 days p.i. In
addition, flow cytometry analysis indicated that T. rangeli infection induces an
early increase in CD11b + Gr1 int cells, suggesting that myeloid cell populations
such as inflammatory monocytes may play a role in controlling infection as well
as the observed persistent inflammation. Consistently, when T. rangeli
trypomastigotes were incubated with murine macrophages, the majority of
parasites were observed outside the cells and no sign of division was detected
for intracellular forms by means of light-microscopy analysis. However, T.
rangeli-exposed macrophages were found to produce high levels of TNF and IL-
6, suggesting that although macrophage sense T. rangeli, controlling of parasite
growth was not completely explained by mononuclear cell recruitment and
activation. We next evaluated the possible role of serum components in T.
rangeli killing. Trypomastigotes treated with normal, but not heat-inactivated,
mouse serum displayed profound changes on parasites morphology as well as
increased propidium iodide staining, indicating serum components participate of
parasite killing. Importantly, pre-treatment of serum with mannose, but not
galactose, blocked the observed T. rangeli killing pointing to a previously