Oral Presentations

Abstract

Galectin-3 (gal-3) has an important role in the inflammatory process, demonstrated by the fact that gal-3 deficient mice (gal3-/-) show decreased recruitment of inflammatory leukocytes in a peritonitis model. In addition, gal-3 is a powerful attractant of monocytes and macrophages. Since leukocyte migration stimulated by lectins was shown to be done through haptotaxis, we investigated if a such mechanism accounts for the human monocyte migration induced by gal-3, as well the participation of components of the extracellular matrix (ECM) in the process. Human monocytes were purified by Ficoll gradient from health voluntaries. The cells were incubated with biotinyl-rgal3 and binding was revealed by streptoavidin-PE. Flow cytometry assays showed that rgal-3 binds to human monocytes, an interaction that was selectively inhibited by lactose. By using Boyden microchamber and Transwell System, we demonstrated that gal-3 induces monocyte migration in a manner that depends on its concentration, as well on its sugar recognition ability. We also showed that the migration is due to a haptotatic mechanism, since the responses to suboptimal doses were increased when the wells were coated with ECM components, especially with laminin and fibronectin. The interaction of rgal-3 and ECM components was confirmed through microplate assays, which demonstrated that binding to laminin is sugar recognition dependent, whereas interaction with fibronectin depends on protein-protein interaction. Galectin-3 induces human monocyte migration through a haptotatic mechanism, a process that involves gal-3 binding to ECM components, such as laminin and fibronectin.