Role of Galectin-3 in Human Pulmonary Fibrosis

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  • Nishi Yumiko
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Sano Hideki
    Department of Internal Medicine, Toho University Sakura Medical Center Department of Allergy and Rheumatology, Chiba-East Hospital, National Hospital Organization
  • Kawashima Tatsuo
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Okada Tomoaki
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Kuroda Toshihisa
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Kikkawa Kyoko
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Kawashima Sayaka
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Tanabe Masaaki
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Goto Tsukane
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Matsuzawa Yasuo
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Matsumura Ryutaro
    Department of Internal Medicine, Toho University Sakura Medical Center Department of Allergy and Rheumatology, Chiba-East Hospital, National Hospital Organization
  • Tomioka Hisao
    Department of Internal Medicine, Toho University Sakura Medical Center
  • Liu Fu-Tong
    Department of Dermatology, University of California, Davis, School of Medicine
  • Shirai Koji
    Department of Internal Medicine, Toho University Sakura Medical Center

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Background: Galectin-3 is a β-galactoside-binding protein which is implicated in diverse physiological and pathological processes including human liver cirrhosis and a mouse lung fibrosis model. The aim of this study is to determine whether galectin-3 is involved in human lung fibrosis.<br> Methods: We measured galectin-3 concentration in bronchoalveolar lavage fluid (BALF) and examined its expression in alveolar macrophages from patients with interstitial lung disorders using ELISA and immunohistochemical staining, respectively. Using monocyte/macrophage cell lines in vitro, we examined the effect of cytokines on galectin-3 expression, and the opposite similarly by RT-PCR and Western blotting. Finally, we performed Micro Boyden chamber assay and Sircoll assay to determine whether galectin-3 induces migration and collagen synthesis, respectively, in fibroblasts.<br> Results: Galectin-3 was specifically increased in BALF from patients with idiopathic pulmonary fibrosis (IPF) and interstitial pneumonia associated with collagen vascular disease (CVD-IP). Galectin-3 levels in BALF seemed to be lower in IPF and CVD-IP patients receiving corticosteroid therapy. Alveolar macrophages from IPF patients expressed more galectin-3 compared with those from control. Galectin-3 expression was induced by tumor necrosis factor-alpha (TNF-α) and interferon (IFN)-γ in a monocytic cell line U937. Galectin-3 also induced mRNA expression and protein production of TNF-α and interleukin (IL)-8 in a macrophage cell line THP-1. This lectin stimulated NIH-3T3 fibroblast to induce migration and collagen synthesis in vitro.<br> Conclusions: These results suggest that galectin-3 is involved in the pathogenesis of human IPF and CVD-IP by activating macrophages and fibroblasts.<br>

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