title: Experimental Chagas disease in Balb/c mice previously vaccinated with T. rangeli. II. The innate immune response shows immunological memory: reality or fiction?
abstract: Trypanosoma cruzi is a real challenge to the host's immune system, because it requires strong humoral and cellular immune response to remove circulating trypomastigote forms, and to prevent the replication of amastigote forms in tissues, involving many regulator and effector components. This protozoan is responsible for Chagas disease, a major public health problem in Latinamerica. We have developed a model of vaccination with Trypanosoma rangeli, a parasite closely related to T. cruzi, but nonpathogenic to humans, which reduces the infectiousness in three different species of animals, mice, dogs and guinea pigs, against challenge with T. cruzi. In a previous work, we demonstrated that mice vaccinated with T. rangeli showed important soluble mediators that stimulate phagocytic activity versus only infected groups. The aim of this work was to study the innate immune response in mice vaccinated or not with T. rangeli. Different population cells and some soluble mediators (cytokines) in peritoneal fluid and plasma in mice vaccinated-infected and only infected with T. cruzi were studied. In the first hours of challenge vaccinated mice showed an increase of macrophages, NK, granulocytes, and regulation of IL6, IFNγ, TNFα and IL10, with an increase of IL12, with respect to only infected mice. Furthermore an increase was observed of Li T, Li B responsible for adaptative response. Finally the findings showed that the innate immune response plays an important role in vaccinated mice for the early elimination of the parasites, complementary with the adaptative immune response, suggesting that vaccination with T. rangeli modulates the innate response, which develops some kind of immunological memory, recognizing shared antigens with T. cruzi. These results could contribute to the knowledge of new mechanisms which would have an important role in the immune response to Chagas disease.
authors.affiliation: 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.forename: B
authors.initials: B
authors.lastname: Basso
authors.affiliation: Department of Immunology Medicine School, Catholic University of Cordoba, Argentina.
authors.forename: V
authors.initials: V
authors.lastname: Marini
mesh_terms: D056704:Adaptive Immunity / Q000276:immunology; D000818:Animals; D000913:Antibodies, Protozoan / Q000097:blood; D000953:Antigens, Protozoan / Q000008:administration & dosage / Q000627:therapeutic use; D014355:Chagas Disease / Q000276:immunology* / Q000517:prevention & control; D056738:Cross Protection / Q000276:immunology; D005260:Female; D006098:Granulocytes / Q000276:immunology; D007113:Immunity, Innate / Q000276:immunology; D007156:Immunologic Memory / Q000276:immunology*; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D018664:Interleukin-12 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007694:Killer Cells, Natural / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018512:Parasitemia / Q000276:immunology / Q000517:prevention & control; D016052:Protozoan Vaccines / Q000276:immunology*; D013154:Spleen / Q000166:cytology / Q000276:immunology; D014349:Trypanosoma cruzi / Q000276:immunology*; D057509:Trypanosoma rangeli / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014611:Vaccination
chemical_list: D000913:Antibodies, Protozoan; D000953:Antigens, Protozoan; C556062:IL10 protein, mouse; D015850:Interleukin-6; D016052:Protozoan Vaccines; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12; D007371:Interferon-gamma
keywords: Experimental Chagas disease; Innate immune response; Peritoneal fluid; Population cells; Trypanosoma cruzi; Trypanosoma rangeli