Macrophages and arginase induction as a mechanism for parasite escape.

CINTHIA STEMPIN, FABIO CERBAN

MEDICINA (BUENOS AIRES)

Fundacion Revista Medicina.

Lugar: Buenos Aires; Año: 2007 vol. 67 p. 737 - 746

0025-7680

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 sensible to nitric oxide (ON) and their derivatives. ON is produced in macrophages (M) after stimulation with microbial products or cytokines. In the past, M were defined as inflammatory cells (classically activated M), able to produce inflammatory mediators, to act like antigens presenting cells and to kill intracellular pathogens. Nevertheless, in the present activated M involve a more heterogeneous group of cells with different biological markers that can carry out different immunological functions. Alternatively activated M fail to produce ON due to the arginase induction and consequently they have diminished its capacity to kill intracellular pathogens. It has been reported the induction of arginase by different parasites; therefore this mechanism could favor its 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 M. 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.