Immunomodulatory effect of B-1 cells and B-1 derived phagocytes (B-1CDP) in experimental Chaga’s Disease by Trypanosoma cruzi
B-1 cells; B-1CDP cells; Trypanosoma cruzi; susceptibility
The hemoflagellate protozoan Trypanosoma cruzi causes Chagas disease; although it has been described over a century ago this disease is still a matter of public health. B-1 cells and/or B-1 phagocyte derived cells (B-1CDP) contribute to the survival of several pathogens. Recent works highlight that over infection by T. cruzi, the B-1 cells execute an immunomodulatory function over phagocytic cells making then more susceptible to the parasite. With this information in mind we decided to evaluate the influence of B-1 and B-1CDP cells during clone Dm28c metacyclic trypomastigotes T. cruzi infection. In parallel, to some cultures were added in the proportion of 10:1 B1 cells to macrophages in vitro. Our results showed that macrophages from BALB/c mice are more susceptible to the T. cruzi infection then macrophage from XID mice. We also demonstrate an increased number of infected cells; with higher numbers of amastigotes forms inside macrophages and more extrusion of trypomastigotes forms. B-1 cells were responsible by the reduction of nitric oxide (NO), influencing the microbicide capacity of this macrophages. The presence of B-1 cells was determinant for the higher susceptibility of BALB/c mice cells and for the brake of tolerance of XID macrophage. In parallel, the B-1 cells induced an increased production of IL-10 cytokine, this one able to modulate the macrophage response to infection by T. cruzi. We also evaluated the possible in vivo effects; and we designed an experiment where BALB/c and XID mice received by adoptive transfer B-1 cells before the intra-peritoneal infection with T.cruzi. Additionally, BALB/c mice that received B-1 cells shown a higher susceptibility when compared with mice that do not received this cells during the course of infection with T.cruzi. Taken together, our work suggests that B-1 and B-1CDP cells contribute leading to decreased resistance favoring parasitism in T. cruzi infection.