Abstract
Trypanosoma cruzi induces inflammatory reactions in several tissues. The production of prostaglandin F2alpha, 6-keto-prostaglandin F1alpha and thromboxane B2, known to regulate the immune response and to participate in inflammatory reactions, was studied in mice experimentally infected with T. cruzi. The generation of nitric oxide (NO), which could be regulated by cyclooxygenase metabolites, was also evaluated. In the acute infection the extension of inflammatory infiltrates in skeletal muscle as well as the circulating levels of cyclooxygenase metabolites and NO were higher in resistant C3H mice than in susceptible BALB/c mice. In addition, the spontaneous release of NO by spleen cells increased earlier in the C3H mouse strain. In the chronic infections, the tissue inflammatory reaction was still prominent in both groups of mice, but a moderate increase of thromboxane B2 concentration and in NO released by spleen cells was observed only in C3H mice. This comparative study shows that these mediators could be mainly related to protective mechanisms in the acute phase, but seem not to be involved in its maintenance in the chronic T. cruzi infections.
Highlights
Trypanosoma cruzi is an intracellular parasite that causes Chagas’ disease, characterized by a progressive inflammatory reaction mainly affecting the function of myocardial and skeletal muscles as well as the visceras of the digestive tract.[1]The murine experimental infections usually show an acute stage with high parasitemia and prominent inflammatory infiltrates in several tissues, including the heart and skeletal muscles.[1]
The aim of this study was to compare the in vivo production of both COX-derived inflammatory mediators and nitric oxide (NO) in BALB/c and C3H mice infected with T. cruzi, Tulahuen strain
In the acute stage of T. cruzi infection, starting by the end of the second week p.i., BALB/c and C3H mice showed a prominent area of inflammatory infiltrates
Summary
Trypanosoma cruzi is an intracellular parasite that causes Chagas’ disease, characterized by a progressive inflammatory reaction mainly affecting the function of myocardial and skeletal muscles as well as the visceras of the digestive tract.[1]. The murine experimental infections usually show an acute stage with high parasitemia and prominent inflammatory infiltrates in several tissues, including the heart and skeletal muscles.[1] At present, the mechanisms that induce this inflammatory reaction and its role in the resistance and/or the outcome of the disease are not fully understood. It could be of interest to characterize the increase of other inflammatory mediators, such as eicosanoids, and their contribution to host defense
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