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Infection and Immunity, March 2006, p. 1580-1587, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1580-1587.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Trypanosoma cruzi Infection and Nuclear Factor Kappa B Activation Prevent Apoptosis in Cardiac Cells

Christine A. Petersen,1* Katherine A. Krumholz,1 John Carmen,2 Anthony P. Sinai,2 and Barbara A. Burleigh1

Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115,1 Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, Kentucky 405362

Received 5 September 2005/ Returned for modification 18 October 2005/ Accepted 20 December 2005

Studies of cardiac pathology and heart failure have implicated cardiomyocyte apoptosis as a critical determinant of disease. Recent evidence indicates that the intracellular protozoan parasite Trypanosoma cruzi, which causes heart disease in chronically infected individuals, impinges on host apoptotic pathways in a cell type-dependent manner. T. cruzi infection of isolated neuronal cells and cardiomyocytes protects against apoptotic cell death, whereas apoptosis is triggered in T cells in T. cruzi-infected animals. In this study, we demonstrate that the ability of T. cruzi to protect cardiac cells in vitro from apoptosis triggered by a combination of tumor necrosis factor alpha and serum reduction correlates with the presence of intracellular parasites and involves activation of host cell NF-{kappa}B. We further demonstrate that the apoptotic block diminishes activation of caspase 3. The ability of T. cruzi to prevent apoptosis of infected cardiomyocytes is likely to play an important role in establishment of persistent infection in the heart while minimizing potential damage and remodeling that is associated with cardiomyocyte apoptosis in cardiovascular disease.

* Corresponding author. Present address: Department of Veterinary Pathology, Rm 2714, College of Veterinary Medicine, Iowa State University, Ames, IA 50014. Phone: (515) 294-9013. Fax: (515) 294-5423. E-mail: kalicat{at}iastate.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, March 2006, p. 1580-1587, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1580-1587.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Lu, X., Liu, H., Wang, L., Schaefer, S. (2009). Activation of NF-{kappa}B is a critical element in the antiapoptotic effect of anesthetic preconditioning. Am. J. Physiol. Heart Circ. Physiol. 296: H1296-H1304 [Abstract] [Full Text]  
  • Cuenca, J., Goren, N., Prieto, P., Martin-Sanz, P., Bosca, L. (2007). Selective Impairment of Nuclear Factor-{kappa}B-Dependent Gene Transcription in Adult Cardiomyocytes: Relevance for the Regulation of the Inflammatory Response in the Heart. Am. J. Pathol. 171: 820-828 [Abstract] [Full Text]  


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