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Infection and Immunity, November 2004, p. 6717-6721, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6717-6721.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Human Galectin-3 Promotes Trypanosoma cruzi Adhesion to Human Coronary Artery Smooth Muscle Cells

Yuliya Y. Kleshchenko,^1, Tapria N. Moody,^1, Vyacheslav A. Furtak,² Josiah Ochieng,² Maria F. Lima,¹ and Fernando Villalta^1*

Department of Microbiology,¹ Department of Biochemistry, School of Medicine, Meharry Medical College, Nashville, Tennessee²

Received 12 May 2004/ Returned for modification 4 July 2004/ Accepted 26 July 2004

Human galectin-3 binds to the surface of Trypanosoma cruzi trypomastigotes and human coronary artery smooth muscle (CASM) cells. CASM cells express galectin-3 on their surface and secrete it. Exogenous galectin-3 increased the binding of T. cruzi to CASM cells. Trypanosome binding to CASM cells was enhanced when either T. cruzi or CASM cells were preincubated with galectin-3. Cells stably transfected with galectin-3 antisense show a dramatic decrease in galectin-3 expression and very little T. cruzi adhesion to cells. The addition of galectin-3 to these cells restores their initial capacity to bind to trypanosomes. Thus, host galectin-3 expression is required for T. cruzi adhesion to human cells and exogenous galectin-3 enhances this process, leading to parasite entry.

Editor: W. A. Petri, Jr.

Y.Y.K. and T.N.M. contributed equally to the present report.

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