| First Author | Gittens BR | Year | 2017 |
| Journal | J Immunol | Volume | 198 |
| Issue | 11 | Pages | 4458-4469 |
| PubMed ID | 28438899 | Mgi Jnum | J:247861 |
| Mgi Id | MGI:5927286 | Doi | 10.4049/jimmunol.1600709 |
| Citation | Gittens BR, et al. (2017) Galectin-3: A Positive Regulator of Leukocyte Recruitment in the Inflamed Microcirculation. J Immunol 198(11):4458-4469 |
| abstractText | In vivo and ex vivo imaging were used to investigate the function of galectin-3 (Gal-3) during the process of leukocyte recruitment to the inflamed microcirculation. The cremasteric microcirculation of wild-type (C57BL/6), Gal-3-/-, and CX3CR1gfp/+ mice were assessed by intravital microscopy after PBS, IL-1beta, TNF-alpha, or recombinant Gal-3 treatment. These cellular responses were investigated further using flow-chamber assays, confocal microscopy, flow cytometry, PCR analysis, and proteome array. We show that mechanisms mediating leukocyte slow rolling and emigration are impaired in Gal-3-/- mice, which could be because of impaired expression of cell adhesion molecules and an altered cell surface glycoproteome. Local (intrascrotal) administration of recombinant Gal-3 to wild-type mice resulted in a dose-dependent reduction in rolling velocity associated with increased numbers of adherent and emigrated leukocytes, approximately 50% of which were Ly6G+ neutrophils. Intrascrotal administration of Gal-3 to CX3CR1gfp/+ mice confirmed that approximately equal numbers of monocytes are also recruited in response to this lectin. Exogenous Gal-3 treatment was accompanied by increased proinflammatory cytokines and chemokines within the local tissue. In conclusion, this study unveils novel biology for both exogenous and endogenous Gal-3 in promoting leukocyte recruitment during acute inflammation. |
