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TNF‐α is expressed at sites of parasite and tissue destruction in the spleen of mice acutely infected with Trypanosoma cruzi
Author(s) -
Lima Elianita Suzart,
Andrade Zilton A.,
Andrade Sonia G.
Publication year - 2001
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1046/j.1365-2613.2001.00203.x
Subject(s) - trypanosoma cruzi , benznidazole , spleen , biology , necrosis , tumor necrosis factor alpha , ratón , monoclonal antibody , kinetoplastida , parasite hosting , immunology , microbiology and biotechnology , virology , antibody , genetics , world wide web , computer science
Mice infected with a macrophagotropic strain of Trypanosoma cruzi develop progressive splenomegaly due to reactive hyperplasia with increased number of lymphocytes and macrophages, culminating in parasite disintegration and necrosis of parasitized cells. Necrotic changes have been attributed to the liberation of toxic cytokines, including TNF‐α, from parasitized macrophages. In the present study, the presence of TNF‐α was investigated in situ . In addition the participation of destroyed parasites in inducing the liberation of TNF‐α was examined in two highly susceptible mice strains (C3H and Swiss) and a more resistant strain (DBA). Swiss (90) C3H/He (83) and DBA (30) mice were infected with the Peruvian strain of T. cruzi . Nineteen infected Swiss mice, and 22 infected C3H/He were treated with Benznidazole (one or two doses, 100 mg/kg bw/day), on the 8th and 9th days after infection . Necrotic splenic lesions occurred in both susceptible and resistant strains of mice. Although differing in degree, lesions were more intense in C3H and Swiss than in DBA mice. Comparing untreated and treated susceptible mice, necrotic lesions were significantly less intense in the latter. By specific monoclonal antibody immunolabelling, TNF‐α was demonstrated in the cytoplasm of macrophages and within necrotic areas, from Swiss, C3H/He and DBA mouse spleens. In conclusion, TNF‐α, probably synthesized by macrophages, was strongly expressed at the sites of parasite and cell destruction, thus appearing to play a pivotal role in splenic necrotic changes associated with severe experimental T. cruzi infection.