Open AccessSilencing of the Laminin γ-1 Gene Blocks Trypanosoma cruzi Infection
Author(s) -
Pius N. Nde,
Katharine B. Simmons,
Yuliya Y. Kleshchenko,
Siddharth Pratap,
Maria F. Lima,
Fernando Villalta
Publication year - 2006
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.74.3.1643-1648.2006
Subject(s) - biology , trypanosoma cruzi , laminin , gene silencing , rna interference , microbiology and biotechnology , chagas disease , gene expression , intracellular , extracellular matrix , virology , gene , parasite hosting , rna , genetics , world wide web , computer science
It is thought thatTrypanosoma 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 theT. cruzi gp83 ligand, a cell surfacetrans -sialidase-like molecule that the parasite uses to attach to host cells, increases the level of laminin γ-1 transcript and its expression in mammalian cells, leading to an increase in cellular infection. Stable RNA interference (RNAi) with host cell laminin γ-1 knocks down the levels of laminin γ-1 transcript and protein expression in mammalian cells, causing a dramatic reduction in cellular infection byT. cruzi . Thus, host laminin γ-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.