title: [Macrophages and arginase induction as a mechanism for parasite escape].
abstract: Although there are several immunological mechanisms to eliminate the intracellular pathogens, they have elaborated a variety of strategies to escape of the immune response and to make possible their survival and replication in the host. Some parasites modulate the production of several toxic molecules synthesized by the immune system. Several parasites are highly sensitive to nitric oxide (ON) and their derivatives. ON is produced in macrophages (Mphi) after stimulation with microbial products or cytokines. In the past, Mphi were defined as inflammatory cells (classically activated Mphi), able to produce inflammatory mediators, to act like antigens presenting cells and to kill intracellular pathogens. Nevertheless, activated Mphi involve a more heterogeneous group of cells with different biological markers that can carry out different immunological functions. Alternatively activated Mphi fail to produce ON due to the arginase induction and consequently they have diminished their capacity to kill intracellular pathogens. It has been reported the induction of arginase by different parasites; therefore this mechanism could favor their survival in the host. In our group, we studied the participation of arginase in a model of Trypanosoma cruzi infection and the intracellular signals involved in the replication of this parasite in Mphi. The data obtained from our works would allow the understanding of some mechanisms by which cells can be programmed to favor the establishment of chronic parasitic infections.
authors.affiliation: Area Inmunología, CIBICI-CONICET, Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: Cinthia C
authors.initials: CC
authors.lastname: Stempin
authors.forename: Fabio M
authors.initials: FM
authors.lastname: Cerban
mesh_terms: D000818:Animals; D000953:Antigens, Protozoan / Q000276:immunology; D001119:Arginase / Q000276:immunology / Q000378:metabolism*; D014355:Chagas Disease / Q000276:immunology*; D004195:Disease Models, Animal; D004790:Enzyme Induction / Q000276:immunology; D007372:Interferons / Q000276:immunology; D007891:Leishmania / Q000254:growth & development; D008262:Macrophage Activation / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000276:immunology; D009569:Nitric Oxide / Q000096:biosynthesis / Q000276:immunology; D014349:Trypanosoma cruzi / Q000254:growth & development*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D000953:Antigens, Protozoan; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D007372:Interferons; D020928:Mitogen-Activated Protein Kinases; D001119:Arginase