title: Experimental Chagas disease. Innate immune response in Balb/c mice previously vaccinated with Trypanosoma rangeli. I. The macrophage shows immunological memory: Reality or fiction?
abstract: Chagas' disease, caused by Trypanosoma cruzi, is a major vector borne health problem in Latin America and an emerging or re-emerging infectious disease in several countries. Immune response to T. cruzi infection is highly complex and involves many components, both regulators and effectors. Although different parasites have been shown to activate different mechanisms of innate immunity, T. cruzi is often able to survive and replicate in its host because they are well adapted to resisting host defences. An experimental model for vaccinating mice with Trypanosoma rangeli, a parasite closely related to T. cruzi, but nonpathogenic to humans, has been designed in our laboratory, showing protection against challenge with T. cruzi infection. The aim of this work was to analyze some mechanisms of the early innate immune response in T. rangeli vaccinated mice challenged with T. cruzi. For this purpose, some interactions were studied between T. cruzi and peritoneal macrophages of mice vaccinated with T. rangeli, infected or not with T. cruzi and the levels of some molecules or soluble mediators which could modify these interactions. The results in vaccinated animals showed a strong innate immune response, where the adherent cells of the vaccinated mice revealed important phagocytic activity, and some soluble mediator (Respiratory Burst: significantly increase, p ≤ 0.03; NO: the levels of vaccinated animals were lower than those of the control group; Arginasa: significantly increase, p ≤ 0.04). The results showed an important role in the early elimination of the parasites and their close relation with the absence of histological lesions that these animals present with regard to the only infected mice. This behaviour reveals that the macrophages act with some type of memory, recognizing the antigens to which they have previously been exposed, in mice were vaccinated with T. rangeli, which shares epitopes with T. cruzi.
authors: Department of Paediatrics, Neonatology Service, Medicine School, National Cordoba University, Argentina; National Co-ordination of Vector Control, Argentina. Electronic address: ebi@fcm.unc.edu.ar.
authors: B
authors: B
authors: Basso
authors: Department of Immunology Medicine School, Catholic University of Cordoba, Argentina.
authors: V
authors: V
authors: Marini
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D014355:Chagas Disease / Q000276:immunology* / Q000469:parasitology; D005260:Female; D006801:Humans; D007113:Immunity, Innate; D007156:Immunologic Memory; D017737:Macrophages, Peritoneal / Q000276:immunology* / Q000469:parasitology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D023421:Models, Animal; D010587:Phagocytosis / Q000276:immunology; D016052:Protozoan Vaccines; D014349:Trypanosoma cruzi / Q000276:immunology*; D057509:Trypanosoma rangeli / Q000276:immunology*; D014611:Vaccination
chemical_list: D016052:Protozoan Vaccines
keywords: Innate immune response; Macrophages; Peritoneal fluid; Trypanosoma cruzi; Trypanosoma rangeli