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Novel insights into the inhibitory effects of Galectin‐1 on neutrophil recruitment under flow
Author(s) -
Cooper Dianne,
Norling Lucy V.,
Perretti Mauro
Publication year - 2008
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1207831
Subject(s) - biology , integrin alpha m , endogeny , flow cytometry , intravital microscopy , endothelium , microbiology and biotechnology , cd18 , inflammation , in vivo , immunology , biochemistry , endocrinology
Galectin‐1 (Gal‐1) is a β‐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‐1β. 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.