Volume 58, Issue 1
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645


Both parasite and host immune factors may contribute to the development and progression of chronic chagasic cardiomyopathy during Trypanosoma cruzi infections. The present study targeted infected children (5-14 years of age) from an endemic area of Paraguay in an analysis of T. cruzi-specific cytokine profiles. This age group is characteristically the most affected by the early phases of infection. Trypanosoma cruzi-induced cytokine gene expression (interleukin-2 [IL-2], and interferon-gamma [IFN-gamma], IL-4, and IL-10) was studied in 25 seropositive children categorized as being either acute, symptomatic, with Romana's sign (n = 2), or early, indeterminate (postacute, n = 23). Acutely infected children showed a distinct T helper cell-1 (Th1)-type (IFN-gamma) cytokine response to infection. The cytokine pattern that was observed in the seropositive, asymptomatic (early, indeterminate) group was of the Th0 type (expression of both IFN-gamma and IL-4). We hypothesize that selective induction of a Th0-type cytokine pattern is important for development of cell-mediated and humoral immune responses that suppress parasite burden, thereby prolonging the onset or limiting the severity of chronic Chagas' disease later in life.

Trypanosoma cruzi, the causative agent of Chagas' disease, is an important cause of heart disease in Latin America. Children are the group most likely to be affected by the early phases of infection. A cross-sectional study conducted in elementary schools in two endemic areas of Paraguay (Potrero and Calle-Poi) detected a T. cruzi seroprevalence of 5.3%. 25 seropositive children in the acute (n = 2) or early indeterminate (n = 23) stage of infection participated in a follow-up study aimed at characterizing the T. cruzi-induced cytokine profile. The acute asymptomatic children showed a distinct T-helper cell-1 (Th1)-type cytokine response to infection with minimal interleukin-4 production, while early indeterminate children showed a pattern of the Th0 type regardless of their parasitemic status. These findings suggest that, once acute symptomatic infections with patent parasitemias are cleared by type 1 immune mechanisms, multiple Th0 responses suppress parasite burdens to subpatent levels as parasites sequester in target organs. Infected persons then remain asymptomatic until the cumulative immunopathogenetic effects of persistent, localized inflammatory responses result in chronic disease.


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