Open AccessEndothelial cell signalling induced by trans ‐sialidase from Trypanosoma cruzi
Author(s) -
Dias Wagner B.,
Fajardo Fernanda D.,
GraçaSouza Aurelio V.,
FreiredeLima Leonardo,
Vieira Fabiana,
Girard Murielle F.,
Bouteille Bernard,
Previato José O.,
MendonçaPreviato Lucia,
Todeschini Adriane R.
Publication year - 2008
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2007.01017.x
Subject(s) - sialidase , trypanosoma cruzi , biology , sialic acid , recombinant dna , enzyme , biochemistry , microbiology and biotechnology , neuraminidase , parasite hosting , gene , world wide web , computer science
Summary The protozoan responsible for Chagas' disease, Trypanosoma cruzi , expresses on its surface an unusual trans ‐sialidase enzyme thought to play an important role in host–parasite interactions. Trans ‐sialidase is the product of a multigene family encoding both active and inactive proteins. We have demonstrated that despite lacking enzymatic activity due to a single mutation, Tyr342‐His, inactive trans ‐sialidase displays sialic acid binding activity, with identical specificity to that of its active analogue. In this work we demonstrate that binding of a recombinant inactive trans ‐sialidase to molecules containing α2,3‐linked sialic acid on endothelial cell surface triggers NF‐κB activation, expression of adhesion molecules and upregulation of parasite entry into host cells. Furthermore, inactive recombinant trans ‐sialidase blocks endothelial cell apoptosis induced by growth factor deprivation. These results suggest that inactive members of the trans ‐sialidase family play a role in endothelial cell responses to T. cruzi infection.