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Glycobiology Advance Access published online on March 24, 2004
Glycobiology, doi:10.1093/glycob/cwh068
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Submitted on January 25, 2004
Revised on February 11, 2004
Accepted on February 24, 2004

© 2004 Glycobiology © Oxford University Press 2004; all rights reserved.

ORIGINAL ARTICLES

Upregulation of galectin-3 and its ligands by Trypanosoma cruzi infection with modulation of adhesion and migration of murine dendritic cells

Bernard Vray 1*, Isabelle Camby 2, Vincent Vercruysse 1, Tatjana Mijatovic 2, Nicolai V. Bovin 3, Paola Ricciardi-Castagnoli 4, Herbert Kaltner 5, Isabelle Salmon 6, Hans-Joachim Gabius 5, and Robert Kiss 2

1 Laboratoire d'Immunologie Expérimentale, Faculté de Médecine, and Laboratoire de Parasitologie, Département de Biologie des Organismes, Faculté des Sciences, Université Libre de Bruxelles, Brussels, Belgium
2 Laboratoire de Toxicologie, Institut de Pharmacie, Université Libre de Bruxelles, Brussels, Belgium
3 Shemyakin Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia
4 Department of Biotechnology and Biosciences, Plaza della Scienza, University of Milano-Bicocca, Milano, Italy
5 Institute of Physiological Chemistry, Faculty of Veterinary Medicine, Ludwig-Maximilians-University, Munich, Germany
6 Service d'Anatomie Pathologique, Hopital Erasme, Université Libre de Bruxelles, Brussels, Belgium

* To whom correspondence should be addressed. E-mail: bvray{at}ulb.ac.be.

Abstract

The impact of a pathogen-induced inflammatory response on dendritic cells (DC) and on their expression of galectin-3 (Gal-3) was studied on splenic DC (sDC) from Trypanosoma cruzi-infected mice. We determined the lectin expression and also presentation of ligands using the labeled galectin as probe. By RT-PCR, Western blot analysis, quantitative glycocytochemistry and computer-assisted quantitative microscopy, we demonstrate that, in sDC from infected mice, expression of Gal-3 and Gal-3-specific ligands were markedly upregulated and adhesiveness was increased with Gal-3 coated substratum. Gal-3 expression was also enhanced in T. cruzi-infected D2SC-1 cells. To assess influence on migration, we had to work exclusively with D2SC-1 cells because sDC rapidly lost their capacity to adhere to substratum. Migration of infected- and TCM-treated D2SC-1 cells were reduced when substratum was coated with Gal-3. Expression of Gal-3 by D2SC-1 was reduced when they were incubated with anti-Gal-3 anti-sense oligonucleotide without effect on cell invasion by the parasite. By using seven neoglycoconjugates, we probed the cellular capacity to specifically bind carbohydrate ligands. Similar to Gal-3, an upregulation was noted with respect to sites specific for Man and {alpha}-GalNAc, respectively, revealing that infection-dependent changes are not confined to Gal-3-dependent parameters. Taken together, these data document for the first time that a parasitic infection can modulate both in vivo and in vitro the expression of Gal-3 and of ligands for this lectin in DC with functional consequences on their capacities of adhesion and migration. These results suggest a new immunomodulatory property of T. cruzi.


galectin-3, glycocytochemistry, spleen murine dendritic cells, neoglycoconjugate, Trypanosoma cruzi
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