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Chapter category: Infectious Disease

Effector Mechanisms of Macrophages Infected with Trypanosoma cruzi

This chapter appears in the following book:

Protozoans in Macrophages

Edited by: Eric Y. Denkers and Ricardo T. Gazzinelli
ISBN: 978-1-58706-150-9
» Get more information about this book at landesbioscience.com «

Chapter authors:
Fredy R.S. Gutierrez, Flavia S. Mariano, Isabel K.F. Miranda-Santos and João S. Silva


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The main effector mechanisms that control infection by T. cruzi depend upon activation of macrophages. These cells are activated soon after infection by mechanisms that are dependent on production of several cytokines and chemokines. Once activated, macrophages, as well other cells of the innate immune system, including cardiomyocytes produce several oxidative molecules, such as nitric oxide. These free radicals kill the intracellular parasites by chemically modifying the structural properties of their proteins and inactivating catalytic sites of their enzymes. Some of these molecules present systemic effects and activate other cells of the innate and adaptive immune responses, recruiting them to the inflammatory site, hence improving the host’s immune response to infection. These energy-consuming responses must be controlled in order to avoid damage to host tissues and macrophages also participate in this aspect of homeostasis. Here we discuss the mechanisms that lead to activation of macrophages, killing of parasites and migration of cells, as well as the consequences of the inflammatory reaction caused by infection with T. cruzi.

Fredy R.S. Gutierrez
Department of Biochemistry and Immunology, School of Medicine of Riberão Preto, University of São Paulo

Flavia S. Mariano
Department of Biochemistry and Immunology, School of Medicine of Riberão Preto, University of São Paulo

Isabel K.F. Miranda-Santos
Department of Biochemistry and Immunology, School of Medicine of Riberão Preto, University of São Paulo

João S. Silva
Department of Biochemistry and Immunology, School of Medicine of Riberão Preto, University of São Paulo

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