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

TUMOR NECROSIS FACTOR MAY CONTRIBUTE TO TRYPANOSOMA
CRUZI PERSISTENCE IN THE CENTRAL NERVOUS SYSTEM FAVORING
ASTROCYTE INFECTION
RAFAEL RODRIGUES SILVA (PG)(1); ANDREA ALICE DA SILVA (1,2);
JOSELI LANNES-VIEIRA (1).
(1).Oswaldo Cruz Institute; (2). Federal Fluminense University
Introduction: The existence of a nervous form in the chronic phase of Chagas
disease is matter of discussion. Trypanosoma cruzi infection of children under
two-year old and immunocompromised patients, with cancer, transplanted or
malnourished, as well as 75-80% cases of co-infected individuals who develop
the acquired immunodeficiency syndrome (AIDS), present immunopathological
alterations in the central nervous system (CNS) with intense parasitism.
Although immunocompetent individuals control T. cruzi dissemination, parasite
persists in the CNS. The mechanisms favoring parasite persistence in an
apparent silence in the nervous tissue, while myocarditis progresses from the
acute to the chronic phase of infection, remain to be understood. Herein, we
approached the participation of tumor necrosis factor (TNF) in the process of
parasite invasion of astrocyte, the main glial cells, studying the infection rates
and the production of nitric oxide (NO). Methods and Results: We used
primary cultures of C3H/He mice astrocytes untreated or treated with TNF prior
to infection with trypomastigote forms of the Colombian strain of T. cruzi.
Interestingly, the astrocyte cultures treated with TNF prior to infection presented
a higher number of intracellular amastigote forms (327.33+3.8 amastigotes/100
cells in TNF-treated cultures vs 219.33+0.94 amastigotes/100 cells in untreated
cultures). TNF also increased the frequency of parasitized astrocytes
(52.31+0.45% in TNF-treated cultures vs 31.15+0.22% in untreated cultures).
Further, the infection rates were dependent on the time of infection and the
multiplicity of infection (MOI). Moreover, independently of previous exposition to
TNF, T. cruzi infection of astrocytes did not induce NO production. Conclusion:
Our data suggest that in the CNS an inflammatory milieu containing TNF may
facilitate the invasion of astrocytes by T. cruzi, which may persist in the nervous
tissue in a silent manner.
Financial support: CAPES, CNPq.