Glycobiology Advance Access originally published online on March 24, 2004
Glycobiology 2004 14(7):647-657; doi:10.1093/glycob/cwh068
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Glycobiology vol. 14 no. 7 © Oxford University Press 2004; all rights reserved.
Up-regulation of galectin-3 and its ligands by Trypanosoma cruzi infection with modulation of adhesion and migration of murine dendritic cells
2 Laboratoire d'Immunologie Expérimentale, Faculté de Médecine, 808 Route de Lennik, 1070 Brussels, and Laboratoire de Parasitologie, Département de Biologie des Organismes, Faculté des Sciences, Université Libre de Bruxelles, Brussels, Belgium; 3 Laboratoire de Toxicologie, Institut de Pharmacie, Université Libre de Bruxelles, Brussels, Belgium; 4 Shemyakin Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia; 5 Department of Biotechnology and Biosciences, Plaza della Scienza, University of Milano-Bicocca, Milano, Italy; 6 Institute of Physiological Chemistry, Faculty of Veterinary Medicine, Ludwig-Maximilians-University, Munich, Germany; and 7 Service d'Anatomie Pathologique, Hopital Erasme, Université Libre de Bruxelles, Brussels, Belgium
Received on January 25, 2004; revised on February 11, 2004; accepted on February 24, 2004
The impact of a pathogen-induced inflammatory response on dendritic cells (DCs) and on their expression of galectin-3 (Gal-3) was studied on splenic DCs (sDCs) from Trypanosoma cruzi–infected mice. We determined the lectin expression and also presentation of ligands using the labeled galectin as probe. By reverse transcriptase polymerase chain reaction, western blot analysis, quantitative glycocytochemistry, and computer-assisted quantitative microscopy, we demonstrate that, in sDCs from infected mice, expression of Gal-3 and Gal-3-specific ligands were markedly up-regulated 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 sDCs 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 antisense 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 up-regulation was noted with respect to sites specific for Man and 
-GalNAc, respectively, revealing that infection-dependent changes are not confined to Gal-3-dependent parameters. Considered 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 DCs with functional consequences on their capacities of adhesion and migration. These results suggest a new immunomodulatory property of T. cruzi.
1 To whom correspondence should be addressed; e-mail: bvray{at}ulb.ac.be
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