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Infection and Immunity, January 2006, p. 135-143, Vol. 74, No. 1
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.1.135-143.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The CC Chemokine Receptor 5 Is Important in Control of Parasite Replication and Acute Cardiac Inflammation following Infection with Trypanosoma cruzi

Jenny L. Hardison,1 Ruth A. Wrightsman,1 Philip M. Carpenter,2 William A. Kuziel,3 Thomas E. Lane,1,4* and Jerry E. Manning1,4

Department of Molecular Biology and Biochemistry,1 Center for Immunology, University of California, Irvine, California 92697,4 Department of Pathology and Laboratory Medicine, University of California at Irvine College of Medicine, Irvine, California 92697,2 Protein Design Labs, Inc., Fremont, California 945553

Received 27 July 2005/ Returned for modification 13 September 2005/ Accepted 28 September 2005

Infection of susceptible mice with the Colombiana strain of Trypanosoma cruzi results in an orchestrated expression of chemokines and chemokine receptors within the heart that coincides with parasite burden and cellular infiltration. CC chemokine receptor 5 (CCR5) is prominently expressed during both acute and chronic disease, suggesting a role in regulating leukocyte trafficking and accumulation within the heart following T. cruzi infection. To better understand the functional role of CCR5 and its ligands with regard to both host defense and/or disease, CCR5–/– mice were infected with T. cruzi, and the disease severity was evaluated. Infected CCR5–/– mice develop significantly higher levels of parasitemia (P ≤ 0.05) and cardiac parasitism (P ≤ 0.01) during acute infection that correlated with reduced survival. Further, we show that CCR5 is essential for directing the migration of macrophages and T cells to the heart early in acute infection with T. cruzi. In addition, data are provided demonstrating that CCR5 does not play an essential role in maintaining inflammation in the heart during chronic infection. Collectively, these studies clearly demonstrate that CCR5 contributes to the control of parasite replication and the development of a protective immune response during acute infection but does not ultimately participate in maintaining a chronic inflammatory response within the heart.

* Corresponding author. Mailing address: Department of Molecular Biology and Biochemistry, 3205 McGaugh Hall, University of California, Irvine, Irvine, CA 92697-3900. Phone: (949) 824-5878. Fax: (949) 824-8551. E-mail: tlane{at}uci.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, January 2006, p. 135-143, Vol. 74, No. 1
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.1.135-143.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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