Production of hydrogen peroxide by peripheral blood monocytes and specific macrophages during experimental infection with Trypanosoma cruzi in vivo

Authors

  • Rossana C.N Melo,

    Corresponding author
    1. Laboratory of Cellular Biology, Institute of Biological Sciences, Federal University of Juiz de Fora (UFJF), 36036-330, Juiz de Fora-MG, Brazil
    Search for more papers by this author
  • Daniela L Fabrino,

    1. Laboratory of Cellular Biology, Institute of Biological Sciences, Federal University of Juiz de Fora (UFJF), 36036-330, Juiz de Fora-MG, Brazil
    Search for more papers by this author
  • Heloisa D'Ávila,

    1. Laboratory of Cellular Biology, Institute of Biological Sciences, Federal University of Juiz de Fora (UFJF), 36036-330, Juiz de Fora-MG, Brazil
    Search for more papers by this author
  • Henrique C Teixeira,

    1. Laboratory of Immunology, Institute of Biological Sciences, Federal University of Juiz de Fora (UFJF), 36036-330, Juiz de Fora-MG, Brazil
    Search for more papers by this author
  • Ana Paula Ferreira

    1. Laboratory of Immunology, Institute of Biological Sciences, Federal University of Juiz de Fora (UFJF), 36036-330, Juiz de Fora-MG, Brazil
    Search for more papers by this author

Corresponding author. Present address: Harvard Medical School/Beth Israel Deaconess Medical Center, DA-617, 330 Brookline Avenue, Boston, MA 002215, USA. Tel.: +1-617-667-3307; fax: +1-617-667-5541 rmelo@bidmc.harvard.edu

Abstract

Acute Chagas' disease triggers potent inflammatory reaction characterized by great increase of peripheral blood monocyte (PBM) and macrophage numbers. We studied the respiratory burst responses of PBM and peritoneal and splenic macrophages to in vivo infection (rats). The ultrastructure of heart inflammatory macrophages was also investigated. The infection increased the hydrogen peroxide (H2O2) production by PBM and splenic macrophages but not by peritoneal macrophages. Accordingly, the PBM and spleen cell numbers increased but the total number of peritoneal cells was similar to controls. Heart macrophages of infected rats exhibited increase (number and size) and activated morphology in parallel to high cardiomyocyte parasitism. Our data highlight the importance of innate immunity and H2O2production to host resistance during acute phase of T. cruzi infection. A novel finding is that H2O2production seems related to specific types of monocytes/macrophages that are able to release this agent when in presence of high parasite load.

Ancillary