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Infection and Immunity, October 2005, p. 6974-6980, Vol. 73, No. 10
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.10.6974-6980.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Toll-Like Receptor 2 Regulates Interleukin-1ß-Dependent Cardiomyocyte Hypertrophy Triggered by Trypanosoma cruzi

Christine A. Petersen, Katherine A. Krumholz, and Barbara A. Burleigh^*

Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115

Received 31 March 2005/ Returned for modification 4 May 2005/ Accepted 2 July 2005

Trypanosoma cruzi, the intracellular protozoan parasite that causes Chagasic cardiomyopathy, elicits a robust hypertrophic response in isolated cardiomyocytes. Previous studies established that T. cruzi-elicited cardiomyocyte hypertrophy is mediated by interleukin-1ß produced by infected cardiomyocyte cultures. Here, we define key upstream signaling events leading to cardiomyocyte hypertrophy in response to T. cruzi infection, to be dependent on Toll-like receptor 2 and NF-B. Furthermore, we demonstrate that cardiomyocyte hypertrophy, which is initiated by live infective T. cruzi trypomastigotes or stimulation of isolated myocytes with secreted/released trypomastigote molecules, is a common outcome of the cardiomyocyte recognition of pathogen-associated molecular patterns by intrinsic Toll-like receptors. This study is the first to link pathogen recognition by intrinsic Toll-like receptors to cardiomyocyte hypertrophy.

Editor: W. A. Petri, Jr.

Present address: Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, IA 50014.

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