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(American Journal of Pathology. 2001;159:1723-1733.)
© 2001 American Society for Investigative Pathology

Regular Articles

Pivotal Role of Interleukin-12 and Interferon-{gamma} Axis in Controlling Tissue Parasitism and Inflammation in the Heart and Central Nervous System during Trypanosoma cruzi Infection

Vladimir Michailowsky*{dagger}, Neide M. Silva*{dagger}, Carolina D. Rocha*, Leda Q. Vieira*, Joseli Lannes-Vieira{ddagger} and Ricardo T. Gazzinelli*{dagger}

From the Department of Biochemistry and Immunology,*
Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte; the Laboratory of Immunopathology,{dagger}
René Rachov Research Center-Oswaldo Cruz Foundation, Belo Horizonte; and the Department of Immunology,{ddagger}
Institute of Oswaldo Cruz-Oswaldo Cruz Foundation, Rio de Janeiro, Brazil

The role of cytokines in the control of tissue parasitism and pathogenesis of experimental Chagas’ disease was investigated. Wild-type and different cytokine as well as inducible nitric oxide synthase (iNOS) knockout mice were infected with the Colombian strain of Trypanosoma cruzi, and the kinetics of tissue parasitism, inflammatory reaction, parasitemia, and mortality were determined. We demonstrate the pivotal role of the interleukin (IL)-12/interferon (IFN)-{gamma}/iNOS axis and the antagonistic effect of IL-4 in controlling heart tissue parasitism, inflammation, and host resistance to acute infection with T. cruzi. Further, the heart and central nervous system were shown the main sites of reactivation of T. cruzi infection in mice lacking functional genes for IFN-{gamma} and IL-12, respectively. Our results also show that in contrast to IFN-{gamma} knockout (KO) mice, splenocytes from IL-12 KO mice infected with T. cruzi produced low levels of IFN-{gamma} upon stimulation with antigen. Consistently, high levels of anti-T. cruzi IgG2a antibodies were detected in the sera from IL-12 KO, but not from IFN-{gamma} KO mice, infected with the Colombian strain of T. cruzi. Thus, our results suggest that the level of IFN-{gamma} deficiency is a major determinant of the site of reactivation of T. cruzi infection in immunocompromised host.




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