Glycoconjugate Journal

, Volume 19, Issue 7, pp 575–581

Galectins as inflammatory mediators


DOI: 10.1023/B:GLYC.0000014088.21242.e0

Cite this article as:
Almkvist, J. & Karlsson, A. Glycoconj J (2002) 19: 575. doi:10.1023/B:GLYC.0000014088.21242.e0


Over the last decade a vast amount of reports have shown that galectin-1 and galectin-3 are important mediators of inflammation. In this review we describe how the galectins may be involved in several parts of the inflammatory process, including the recruitment of neutrophils into an infected tissue and the recognition and killing of bacteria by activation of the tissue destructive phagocytic respiratory burst. During bacterial infection or aseptic inflammatory processes, galectins are produced and released by e.g. infected epithelium, activated tissue-resident macrophages and endothelial cells. These extracellular galectins may facilitate binding of neutrophils to the endothelium by cross-linking carbohydrates on the respective cells. Further the galectins improve binding of the neutrophil to the extracellular matrix proteins laminin and fibronectin, and are potential chemotactic factors, inducing migration through the extracellular matrix towards the inflammatory focus. When the cells encounter bacteria, galectin-3 could function as an opsonin, cross-linking bacterial lipopolysaccharide or other carbohydrate-containing surface structures to phagocyte surface glycoconjugates. Both galectin-1 and galectin-3 have the capacity to induce a respiratory burst in neutrophils, provided that the cells have been primed by degranulation and receptor upregulation. The reactive oxygen species produced may be destructive to the invading micro-organisms as well as to the surrounding host tissue, pointing out the possible role of galectins, not only in defence toward infection, but also in inflammatory-induced tissue destruction. Published in 2004.

neutrophilgalectin-1galectin-3transmigrationrespiratory burstinflammation

Copyright information

© Kluwer Academic Publishers 2002

Authors and Affiliations

  1. 1.The Phagocyte Research Laboratory, Department of Rheumatology and Inflammation ResearchGöteborg UniversitySweden