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 journalArticle

109 Citations (Scopus)

Abstract

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
Volume56
Issue number1
DOIs
StatePublished - Mar 2007

Fingerprint

Galectin 3
Pulmonary Fibrosis
Idiopathic Pulmonary Fibrosis
Bronchoalveolar Lavage Fluid
Fibroblasts
Macrophages
Alveolar Macrophages
Cell Line
Lung
Fibrosis
human galectin-3
Collagen
Tumor Necrosis Factor-alpha
Physiological Phenomena
Galactosides
Collagen Diseases
Interstitial Lung Diseases
Pathologic Processes
Interleukin-8
Vascular Diseases

Keywords

  • Angiogenesis
  • Chemokine
  • Cytokine
  • Lectins
  • Pulmonary fibrosis

ASJC Scopus subject areas

  • Immunology and Allergy

Cite this

Nishi, Y., Sano, H., Kawashima, T., Okada, T., Kuroda, T., Kikkawa, K., ... Shirai, K. (2007). Role of galectin-3 in human pulmonary fibrosis. Allergology International, 56(1), 57-65. https://doi.org/10.2332/allergolint.O-06-449

Role of galectin-3 in human pulmonary fibrosis. / Nishi, Yumiko; Sano, Hideki; Kawashima, Tatsuo; Okada, Tomoaki; Kuroda, Toshihisa; Kikkawa, Kyoko; Kawashima, Sayaka; Tanabe, Masaaki; Goto, Tsukane; Matsuzawa, Yasuo; Matsumura, Ryutaro; Tomioka, Hisao; Liu, Fu-Tong; Shirai, Koji.

In: Allergology International, Vol. 56, No. 1, 03.2007, p. 57-65.

Research output: Contribution to journalArticle

Nishi, Y, Sano, H, Kawashima, T, Okada, T, Kuroda, T, Kikkawa, K, Kawashima, S, Tanabe, M, Goto, T, Matsuzawa, Y, Matsumura, R, Tomioka, H, Liu, F-T & Shirai, K 2007, 'Role of galectin-3 in human pulmonary fibrosis', Allergology International, vol. 56, no. 1, pp. 57-65. https://doi.org/10.2332/allergolint.O-06-449
Nishi Y, Sano H, Kawashima T, Okada T, Kuroda T, Kikkawa K et al. Role of galectin-3 in human pulmonary fibrosis. Allergology International. 2007 Mar;56(1):57-65. https://doi.org/10.2332/allergolint.O-06-449
Nishi, Yumiko ; Sano, Hideki ; Kawashima, Tatsuo ; Okada, Tomoaki ; Kuroda, Toshihisa ; Kikkawa, Kyoko ; Kawashima, Sayaka ; Tanabe, Masaaki ; Goto, Tsukane ; Matsuzawa, Yasuo ; Matsumura, Ryutaro ; Tomioka, Hisao ; Liu, Fu-Tong ; Shirai, Koji. / Role of galectin-3 in human pulmonary fibrosis. In: Allergology International. 2007 ; Vol. 56, No. 1. pp. 57-65.
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AU - Sano, Hideki

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AU - Okada, Tomoaki

AU - Kuroda, Toshihisa

AU - Kikkawa, Kyoko

AU - Kawashima, Sayaka

AU - Tanabe, Masaaki

AU - Goto, Tsukane

AU - Matsuzawa, Yasuo

AU - Matsumura, Ryutaro

AU - Tomioka, Hisao

AU - Liu, Fu-Tong

AU - Shirai, Koji

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N2 - 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.

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KW - Chemokine

KW - Cytokine

KW - Lectins

KW - Pulmonary fibrosis

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