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(American Journal of Pathology. 2000;156:1073-1083.)
© 2000 American Society for Investigative Pathology

Regular Articles

Targeted Disruption of the Galectin-3 Gene Results in Attenuated Peritoneal Inflammatory Responses

Daniel K. Hsu*, Ri-Yao Yang*, Zhixing Pan{dagger}, Lan Yu*, Daniel R. Salomon{dagger}, Wai-Ping Fung-Leung{ddagger} and Fu-Tong Liu*

From the Division of Allergy,*
La Jolla Institute for Allergy and Immunology, San Diego, California; the Department of Molecular and Experimental Medicine,{dagger}
the Scripps Research Institute, La Jolla, California; and the R.W. Johnson Pharmaceutical Research Institute,{ddagger}
La Jolla, California

Galectin-3 is a member of a growing family of ß-galactoside-binding animal lectins. Previous studies have demonstrated a variety of biological activities for this protein in vitro, including activation of cells, modulation of cell adhesion, induction of pre-mRNA splicing, and regulation of apoptosis. To assist in fully elucidating the physiological and pathological functions of this protein, we have generated galectin-3-deficient (gal3-/-) mice by targeted interruption of the galectin-3 gene. Gal3-/- mice consistently developed fewer inflammatory cell infiltrations in the peritoneal cavities than the wild-type (gal3+/+) mice in response to thioglycollate broth treatment, mainly due to lower numbers of macrophages. Also, when compared to cells from gal3+/+ mice, thioglycollate-elicited inflammatory cells from gal3-/- mice exhibited significantly lower levels of NF-{kappa}B response. In addition, dramatically different cell-spreading phenotypes were observed in cultured macrophages from the two genotypes. Whereas macrophages from gal3+/+ mice exhibited well spread out morphology, those from gal3-/- mice were often spindle-shaped. Finally, we found that peritoneal macrophages from gal3-/- mice were more prone to undergo apoptosis than those from gal3+/+ mice when treated with apoptotic stimuli, suggesting that expression of galectin-3 in inflammatory cells may lead to longer cell survival, thus prolonging inflammation. These results strongly support galectin-3 as a positive regulator of inflammatory responses in the peritoneal cavity.




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