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(American Journal of Pathology. 2004;165:2045-2053.)
© 2004 American Society for Investigative Pathology

Critical Role for Galectin-3 in Airway Inflammation and Bronchial Hyperresponsiveness in a Murine Model of Asthma

Riaz I. Zuberi*, Daniel K. Hsu{dagger}, Omer Kalayci{ddagger}, Huan-Yuan Chen{dagger}, Holly K. Sheldon{ddagger}, Lan Yu{dagger}, John R. Apgar§, Toshiaki Kawakami*, Craig M. Lilly{ddagger} and Fu-Tong Liu{dagger}

From the Division of Allergy,* La Jolla Institute for Allergy and Immunology, San Diego, California; the Department of Dermatology,{dagger} University of California, Davis, School of Medicine, Sacramento, California; the Department of Molecular and Experimental Medicine,§ The Scripps Research Institute, La Jolla, California; and the Department of Medicine,{ddagger} Harvard Medical School, Brigham and Women’s Hospital, Boston, Massachusetts

Galectin-3 is a member of a ß-galactoside-binding animal lectin family. Previous in vitro studies have demonstrated that galectin-3 is involved in a number of activities; however, the roles of this lectin in physiological and pathological processes in vivo remain to be elucidated. Herein, we show, in a murine model of ovalbumin (OVA)-induced asthma that 1) peribronchial inflammatory cells expressed large amounts of galectin-3; 2) bronchoalveolar lavage fluid from OVA-challenged mice contained significantly higher levels of galectin-3 compared to control mice; and 3) macrophages in bronchoalveolar lavage fluid were the major cell type that contained galectin-3. We investigated the role of galectin-3 in the allergic airway response by comparing galectin-3-deficient (gal3–/–) mice and wild-type (gal3+/+) mice. OVA-sensitized gal3–/– mice developed fewer eosinophils and lower goblet cell metaplasia, after airway OVA challenge compared to similarly treated gal3+/+ mice. In addition, the OVA-sensitized gal3–/– mice developed significantly less airway hyperresponsiveness after airway OVA challenge compared to gal3+/+ mice. Finally, gal3–/– mice developed a lower Th2 response, but a higher Th1 response, suggesting that galectin-3 regulates the Th1/Th2 response. We conclude that galectin-3 may play an important role in the pathogenesis of asthma and inhibitors of this lectin may prove useful for treatment of this disease.




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