Absence of Interferon-γ–Inducible Gene IGTP Does Not Significantly Alter the Development of Chagasic Cardiomyopathy in Mice Infected with Trypanosoma cruzi (Brazil Strain)

Authors

A. P. de Souza, Albert Einstein College of Medicine, Bronx, New York
B. Tang, Albert Einstein College of Medicine, Bronx, New York
H. B. Tanowitz, Albert Einstein College of Medicine, Bronx, New York
S. M. Factor, Albert Einstein College of Medicine, Bronx, New York
V. Shtutin, Albert Einstein College of Medicine, Bronx, New York
J. Shirani, Albert Einstein College of Medicine, Bronx, New York
G. A. Taylor, Duke University, Durham, North Carolina
L. M. Weiss, Albert Einstein College of Medicine, Bronx, New York
L. A. Jelicks, Albert Einstein College of Medicine, Bronx, New York

Date of this Version

2003

Comments

Published in J. Parasitol., 89(6), 2003, pp. 1237–1239.

Abstract

Interferon-γ (IFN-γ) contributes to host resistance during acute infection with Trypanosoma cruzi, the causative agent of Chagas’ disease. Inducibly expressed guanosine triphosphatase (IGTP), a 48-kDa guanosine triphosphatase (GTPase), is a member of a family of GTPase proteins inducibly expressed by IFN-γ. The expression pattern of IGTP suggests that it may mediate IFN-γ–induced responses in a variety of cell types. IGTP has been demonstrated to be important for control of Toxoplasma gondii infection but not for resistance against Listeria monocytogenes. We evaluated the role of IGTP in development of chronic chagasic cardiomyopathy in IGTP null mice and C57X129sv (wild type [WT]) mice infected with the Brazil strain for 6 mo. There was no significant difference in parasitemia or cardiac histopathology between null and WT mice. Right ventricular remodeling was observed in infected IGTP null mice, suggesting that IGTP does not significantly alter the course of T. cruzi infection.