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Glycobiology Advance Access published online on October 10, 2008
Glycobiology, doi:10.1093/glycob/cwn104
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Communications

Galectin-3 functions as an opsonin and enhances macrophage clearance of apoptotic neutrophils

Anna Karlsson1,*, Karin Christenson1,*, Mustafa Matlak1, Åse Björstad1, Kelly L. Brown1, Esbjörn Telemo1, Emma Salomonsson2, Hakon Leffler2 and Johan Bylund1,{dagger}

1 Department of Rheumatology and Inflammation Research, University of Gothenburg, Sweden
2 Section for Microbiology, Immunology, Glycobiology, Department of Laboratory Medicine, University of Lund, Sweden

{dagger} Correspondence to: Johan Bylund, Department of Rheumatology and Inflammation Research, Guldhedsgatan 10, S-413 46 Gothenburg, Sweden, Phone +46–31-342 46 85; E-mail: Johan.Bylund{at}rheuma.gu.se

Received on April 14, 2008; accepted on September 30, 2008

Galectin-3, a β-galactoside binding, endogenous lectin, takes part in various inflammatory events and is produced in substantial amounts at inflammatory foci. We investigated whether extracellular galectin-3 could participate in phagocytic clearance of apoptotic neutrophils by macrophages, a process of crucial importance for termination of acute inflammation. Using human leukocytes, we show that exogenously added galectin-3 increased the uptake of apoptotic neutrophils by monocyte-derived macrophages (MDM). Both the proportion of MDM that engulfed apoptotic prey, as well as the number of apoptotic neutrophils that each MDM engulfed, was enhanced in the presence of galectin-3. The effect was lactose-inhibitable and required galectin-3 affinity for N-acetyllactosamine, a saccharide typically found on cell surface glycoproteins, since a mutant lacking this activity was without effect. The enhanced uptake relied on the presence of galectin-3 during cellular interaction, and was paralleled by lectin binding to apoptotic cells as well as MDM in a lactose-dependent manner. These findings suggest that galectin-3 functions as a bridging molecule between phagocyte and apoptotic prey, acting as an opsonin. The process of clearance, whereby apoptotic neutrophils are removed by macrophages, is crucial for the resolution of acute inflammation and our data imply that the increased levels of galectin-3 often found at inflammatory sites could potently affect this process.

Key words: clearance / inflammation / mdm / phagocytosis

* Equal contribution.


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