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Investigating Novel Roles for Exogenous and Endogenous Galectin‐3 in Controlling Vascular Inflammation
Author(s) -
Gittens Beatrice,
Perretti Mauro,
Cooper Dianne
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.138.12
Subject(s) - intravital microscopy , inflammation , galectin , endogeny , integrin alpha m , downregulation and upregulation , immunology , chemistry , recombinant dna , microcirculation , microbiology and biotechnology , biology , medicine , endocrinology , flow cytometry , biochemistry , gene
Studies in Galectin‐3 (Gal‐3) null mice indicate a role for this β‐ galactoside‐binding lectin in β2integrin‐independent neutrophil recruitment, whilst the recombinant protein induces L‐Selectin shedding and CD11b upregulation in naïve and primed neutrophils. However, its role in leukocyte trafficking in β2‐dependent models has not been systematically addressed. Intravital microscopy of the cremaster muscle was performed in C57BL/6 (WT) or Gal‐3 null mice, following intrascrotal injection of PBS, IL‐1β (30ng), TNF‐α (300ng) or Gal‐3 (200–1000ng) and intravenous administration of anti‐Ly6G to label neutrophils. Treatment with IL‐1β and TNF‐α significantly reduced leukocyte rolling velocities in WT mice, an effect that was absent in Gal‐3 null mice. In addition, a significant reduction in cell emigration was observed in the Gal‐3 null mice treated with IL‐1β. Administration of Gal‐3 to WT mice resulted in a significant reduction in rolling velocity associated with increased numbers of adherent and emigrated leukocytes, approximately 50% of which were Ly6G‐positive neutrophils. These data suggest that Gal‐3 positively regulates leukocyte recruitment in a stimulus dependent fashion in the inflamed microcirculation. This study unveils novel biology for exogenous and endogenous Gal‐3 in controlling vascular inflammation. Supported by British Heart Foundation Studentship FS/10/009/28166