Role of galectin-3 in human pulmonary fibrosis

Yumiko Nishi, Hideki Sano, Tatsuo Kawashima, Tomoaki Okada, Toshihisa Kuroda, Kyoko Kikkawa, Sayaka Kawashima, Masaaki Tanabe, Tsukane Goto, Yasuo Matsuzawa, Ryutaro Matsumura, Hisao Tomioka, Fu-Tong Liu, Koji Shirai

Research output: Contribution to journalArticlepeer-review

140 Scopus citations


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. 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. 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. Conclusions: These results suggest that galectin-3 is involved in the pathogenesis of human IPF and CVD-IP by activating macrophages and fibroblasts.

Original languageEnglish (US)
Pages (from-to)57-65
Number of pages9
JournalAllergology International
Issue number1
StatePublished - Mar 2007


  • Angiogenesis
  • Chemokine
  • Cytokine
  • Lectins
  • Pulmonary fibrosis

ASJC Scopus subject areas

  • Immunology and Allergy


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