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Am. J. Trop. Med. Hyg., 79(5), 2008, pp. 760-767
Copyright © 2008 by The American Society of Tropical Medicine and Hygiene

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A Magnetic Resonance Imaging Study of Intestinal Dilation in Trypanosoma cruzi–infected Mice Deficient in Nitric Oxide Synthase

Lars Ny, Hua Li, Shankar Mukherjee, Katarina Persson, Bo Holmqvist, Dazhi Zhao, Vitaliy Shtutin, Huan Huang, Louis M. Weiss, Fabiana S. Machado, Stephen M. Factor, John Chan, Herbert B. Tanowitz*, AND Linda A. Jelicks
Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden; Departments of Physiology and Biophysics, Pathology, Medicine, and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; School of Pure and Applied Natural Sciences, University of Kalmar, Kalmar, Sweden; Department of Pathology, Lund University Hospital, Lund, Sweden; Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio; Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil

Infection with Trypanosoma cruzi causes megasyndromes of the gastrointestinal (GI) tract. We used magnetic resonance imaging (MRI) to monitor alterations in the GI tract of T. cruzi–infected mice, and to assess the role of nitric oxide (NO) in the development of intestinal dilation. Brazil strain–infected C57BL/6 wild-type (WT) mice exhibited dilatation of the intestines by 30 days post-infection. Average intestine lumen diameter increased by 72%. Levels of intestinal NO synthase (NOS) isoforms, NOS2 and NOS3, were elevated in infected WT mice. Inflammation and ganglionitis were observed in all infected mice. Intestinal dilation was observed in infected WT, NOS1, NOS2, and NOS3 null mice. This study demonstrates that MRI is a useful tool to monitor intestinal dilation in living mice and that these alterations may begin during acute infection. Furthermore, our data strongly suggests that NO may not be the sole contributor to intestinal dysfunction resulting from this infection.


Received May 6, 2008. Accepted for publication July 12, 2008.

Financial support: This study was supported by the Swedish Foundation for Strategic Research and grants from the United States National Institutes of Health (AI-062730 (LAJ), AHA SDG 0735252N (SM), AI052739, AI058893 (HH), and AI068538 (HBT).

Disclaimer: All authors have no conflict of interest.

* Address correspondence to Herbert B. Tanowitz, Departments of Pathology and Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461. E-mail: tanowitz{at}aecom.yu

Authors’ addresses: Lars Ny, Department of Oncology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden. Hua Li and Linda A. Jelicks, Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, NY 10461. Shankar Mukherjee, Dazhi Zhao, Vitaliy Shtutin, and Huan Huang, Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461. Katarina Persson, School of Pure and Applied Natural Sciences, University of Kalmar, SE-391 82 Kalmar, Sweden. Bo Holmqvist, Department of Pathology, Lund University Hospital, SE-221 85 Lund, Sweden. Louis M. Weiss, Stephen M. Factor, and Herbert B. Tanowitz, Departments of Pathology and Medicine, Albert Einstein College of Medicine, Bronx, NY 10461. Fabiana S. Machado, Division of Molecular Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH and the Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Brazil. John Chan, Departments of Microbiology and Immunology and Medicine, Albert Einstein College of Medicine, Bronx, NY 10461. Reprint requests: Herbert B. Tanowitz, Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, E-mail: tanowitz{at}aecom.yu.edu.




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J. L. Durand, S. Mukherjee, F. Commodari, A. P. De Souza, D. Zhao, F. S. Machado, H. B. Tanowitz, and L. A. Jelicks
Role of NO Synthase in the Development of Trypanosoma cruzi-Induced Cardiomyopathy in Mice
Am J Trop Med Hyg, May 1, 2009; 80(5): 782 - 787.
[Abstract] [Full Text] [PDF]




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