Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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A more recent version of this article appeared on June 1, 2008

Published online before print March 27, 2008
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1207831

Received for publication December 14, 2007.
Revised February 8, 2008.
Accepted for publication February 25, 2008.

Article

Novel insights into the inhibitory effects of Galectin-1 on neutrophil recruitment under flow

Dianne Cooper @, Lucy V. Norling , and Mauro Perretti

William Harvey Research Institute, Barts and The London, London, United Kingdom

@ To whom correspondence should be addressed. E-mail: d.cooper{at}qmul.ac.uk.


  Abstract

Galectin-1 (Gal-1) is a {beta}-galactoside-binding protein endowed with anti-inflammatory properties. The purpose of this study was to investigate the effects of endogenous and exogenous Gal-1 on neutrophil recruitment onto TNF-treated endothelium. The effect of human recombinant (hr)Gal-1 on markers of neutrophil activation (CD11b expression, P-selectin glycoprotein ligand 1, and L-selectin shedding) was also assessed. Gal-1 inhibited the platelet-activating factor-induced increase in CD11b expression in a concentration-dependent manner, as assessed by flow cytometry. To determine the effects of Gal-1 on neutrophil recruitment, an in vitro flow chamber was used: Preincubation of neutrophils with hrGal-1 significantly decreased the extent of capture, rolling, and adhesion on activated endothelial monolayers. This inhibition was shared with the endogenous protein, as knockdown of endothelial Gal-1 using small interfering RNA resulted in a significant increase in the number of cells captured and rolling. To verify the effects of Gal-1 in an in vivo system, intravital microscopy of Gal-1 null mice and their wild-type counterparts was performed. Leukocyte adhesion and emigration were increased significantly in the cremasteric circulation of Gal-1 null mice inflamed with IL-1{beta}. These findings indicate that Gal-1 functions to limit neutrophil recruitment onto a TNF-treated endothelium, a property that may underline its inhibitory effects in acute inflammation.

Key Words: endothelial cells • inflammation • adhesion molecules






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Copyright © 2008 by the Society for Leukocyte Biology.