This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nde, P. N.
Right arrow Articles by Villalta, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nde, P. N.
Right arrow Articles by Villalta, F.

 Previous Article  |  Next Article 

Infection and Immunity, March 2006, p. 1643-1648, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1643-1648.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Silencing of the Laminin {gamma}-1 Gene Blocks Trypanosoma cruzi Infection

Pius N. Nde,{dagger} Kaneatra J. Simmons,{dagger} Yuliya Y. Kleshchenko, Siddharth Pratap, Maria F. Lima, and Fernando Villalta*

Division of Microbial Pathogenesis and Immune Response, Department of Biomedical Sciences, School of Medicine, Meharry Medical College, Nashville, Tennessee 37208

Received 31 October 2005/ Returned for modification 5 December 2005/ Accepted 28 December 2005

It is thought that Trypanosoma cruzi, the protozoan that causes Chagas' disease, modulates the extracellular matrix network to facilitate infection of human cells. However, direct evidence to document this phenomenon is lacking. Here we show that the T. cruzi gp83 ligand, a cell surface trans-sialidase-like molecule that the parasite uses to attach to host cells, increases the level of laminin {gamma}-1 transcript and its expression in mammalian cells, leading to an increase in cellular infection. Stable RNA interference (RNAi) with host cell laminin {gamma}-1 knocks down the levels of laminin {gamma}-1 transcript and protein expression in mammalian cells, causing a dramatic reduction in cellular infection by T. cruzi. Thus, host laminin {gamma}-1, which is regulated by the parasite, plays a crucial role in the early process of infection. This is the first report showing that knocking down the expression of a human gene by RNAi inhibits the infection of an intracellular parasite.

* Corresponding author. Mailing address: Division of Microbial Pathogenesis and Immune Response, Department of Biomedical Sciences, School of Medicine, Meharry Medical College, 1005 Dr. D. B. Todd Jr. Blvd., Nashville, TN 37208. Phone: (615) 327-6667. Fax: (615) 327-6072. E-mail: fvillalta{at}mmc.edu.

Editor: W. A. Petri, Jr.

{dagger} P.N.N. and K.J.S. contributed equally to this work.

Infection and Immunity, March 2006, p. 1643-1648, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1643-1648.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Madison, M. N., Kleshchenko, Y. Y., Nde, P. N., Simmons, K. J., Lima, M. F., Villalta, F. (2007). Human Defensin {alpha}-1 Causes Trypanosoma cruzi Membrane Pore Formation and Induces DNA Fragmentation, Which Leads to Trypanosome Destruction. Infect. Immun. 75: 4780-4791 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»