Congenital Transmission ofTrypanosoma cruziIs Associated with Maternal Enhanced Parasitemia and Decreased Production of Interferon‐γ in Response to Parasite Antigens
Author(s) -
Emmanuel Hermann,
Carine Truyens,
Cristina AlonsoVega,
Patricia Rodríguez,
Aurélie Berthe,
Faustino Torrico,
Yves Carlier
Publication year - 2004
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/382511
Subject(s) - parasitemia , trypanosoma cruzi , parasite hosting , virology , antigen , chagas disease , immunology , transmission (telecommunications) , biology , interferon , interferon gamma , protozoa , plasmodium falciparum , microbiology and biotechnology , malaria , immune system , world wide web , computer science , electrical engineering , engineering
The conditions and mechanisms of congenital transmission of Trypanosoma cruzi remain largely unknown. In the present study, we compared the parasitic loads and the immune responses of pregnant T. cruzi-infected women who transmitted parasites to their fetus ("M+B+ mothers") with those of such women who did not transmit parasites to their fetus ("M+B- mothers"). M+B+ mothers had a higher frequency of positive results of hemoculture for T. cruzi than did M+B- mothers, in association with depressed production of parasite-specific interferon- gamma by blood cells that persisted after delivery. In contrast, the production of interleukin (IL)-2, IL-4, and IL-10 and transforming growth factor- beta 1 was similar between both groups of infected mothers, after stimulation with T. cruzi lysate. Flow cytometric analysis showed that T cells and monocytes of M+B+ mothers were less activated than were those of M+B- mothers. Altogether, these results indicate that congenital transmission of T. cruzi is associated with high parasitic loads and peripheral deficient immunological responses in mothers.
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