. Finally, daily treatment of infected mice with CP-105,696 was accompanied by a significantly higher level of blood parasitemia, but not lethality, than that seen in vehicle-treated animals. In conclusion, our results suggest a role for LTB 4 during experimental T. cruzi infection. Chemoattractant molecules such as LTB 4 not only may play a major role in leukocyte migration into sites of inflammation in vivo but also, in the event of an infection, may play a relevant role in the activation of recruited leukocytes to kill the invading microorganism in an NO-dependent manner.Chagas' disease is a protozoan infection caused by Trypanosoma cruzi and is an important public health problem in much of Latin America. The murine model of Chagas' disease has been used to understand the pathophysiological mechanisms underlying the disease and host protection. In this model, host resistance developed against parasites is dependent on the production of inflammatory cytokines, especially interleukin-12, which triggers the production of gamma interferon (IFN-␥) by NK or T cells, and tumor necrosis factor alpha (TNF-␣) (1, 5-7). These cytokines can in turn activate macrophages to produce nitric oxide (NO), the main effector molecule that controls intracellular parasite replication (5, 10, 15, 31). In macrophages, NO is generated from the guanidino nitrogen atom of L-arginine by an inducible NADPH-dependent enzyme called inducible NO synthase (iNOS) (19,22). More recently, it was shown that chemoattractant molecules which act on G protein-coupled serpentine receptors, such as chemokines and platelet-activating factor (PAF), may also participate in the cascade of events leading to NO production and parasite killing (2, 3). On the other hand, interleukin-10 and transforming growth factor  appear to modulate negatively the production of NO and T. cruzi killing induced by proinflammatory cytokines (28,29).Leukotrienes are metabolites of arachidonic acid and have been shown to induce leukocyte activation and/or recruitment in several models of inflammation (9, 14). Leukotriene B 4 (LTB 4 ) acts via G protein-coupled receptors and is enzymatically produced through the 5-lipoxygenase pathway (8,33). A previous study demonstrated the ability of LTB 4 to induce the uptake and killing of T. cruzi by murine macrophages (32). However, the mechanisms underlying LTB 4 -induced killing and whether this was relevant in vivo were not evaluated. Here we investigated the ability of LTB 4 to induce the production of NO and whether NO mediated LTB 4 -induced parasite killing by peritoneal macrophages infected with T. cruzi in vitro. As the actions of LTB 4 may be partially dependent on the release of secondary mediators, such as PAF (13,16,18,24), we also evaluated whether LTB 4 -induced NO production and parasite killing were PAF dependent. Finally, we investigated whether endogenous production of LTB 4 played a relevant role in the infection of mice with T. cruzi in vivo.