The release of reactive oxygen intermediates(ROl), mediators of inflammatory reactions, was evaluated in murine Trypanosoma cruzi infection. In acutely infected BALBIC mice, spleen cells were stimulated, either with epimastigote or trypomastigote forms of the parasite, and the effect was enhanced by serum from infected mice. Only opsonized parasites triggered the release of ROI by normal mouse cells and this response was several times lower than in infected mice. This seems to indicate that cells from acutely infected mice reacted to T. cruzi and that neither parasites nor serum factors blocked the release of ROl. During the acute stage of the infection, both the parasitemia and the release of ROI by spleen cells were higher in BALB/c than in C3H mice (ROI generated in response to a phagocytic stimulation was 12 and 3 times the normal levels, respectively). In addition, in BALB/c mice infected with different numbers of parasites, the production of ROl was related to parasitemia. On the other hand, during the chronic stage of the infection, the inflammatory reaction in myocardium was greater in C3H than in BALB/c mice, and the increase in ROl production was 30% and 100% above the normal levels in BALB/c and C3H mice, respec tively. This suggests that the increased ROI production paralleled the parasite burden in the acute phase, and could be related to inflammatory processes after the control of the parasitemia.

During acute Trypanosoma cruzi infections, macrophages increase phagocytic'and trypanocidal activities. 2 This ac tivation of phagocytic cells is considered important for host defense mechanism (s) against T. ru23 the causative agent of Chagas' disease. In murmneexperimental infections, in vivo treatment with the phagocytic cell activator interferon., Y (WN-@ y) increases the resistance to infection. 4 In vitro, spleen cells from infected mice incubated with specific an tigens release cytokine (s) that activate the trypanocidab ac tivity of phagocytic cells. 5 The amount and rate of the lym phokines produced by cells from different strains of mice correlates with the host strain resistance to the infection. 5 These observations suggest that the enhanced trypanocidal activity of phagocytic cells by T cell-derived lymphokines is an immune effector mechanism for the control of T. cruzi infections. 5