title: A possible role of galectin-9 in the pulmonary fibrosis of patients with interstitial pneumonia.
abstract: BACKGROUND
  Galectin-9 (Gal-9) is a β-galactoside-binding protein that induces biological reactions, such as cell activation, chemoattraction, and apoptosis. We evaluated the role of Gal-9 in the pathogenesis of interstitial pneumonia (IP).
  
  
  METHODS
  Gal-9 levels in the bronchoalveolar lavage fluid (BALF) of patients with IP associated with collagen vascular disease (CVD-IP) and with idiopathic interstitial pneumonias (IIPs), including idiopathic pulmonary fibrosis (IPF) and idiopathic nonspecific interstitial pneumonia (idiopathic NSIP), were estimated by enzyme-linked immunosorbent assay. Gal-9 expression in the lungs of these patients was evaluated using immunohistochemistry. The effect of Gal-9 on the growth and apoptosis of human lung fibroblast cells was assessed in vitro.
  
  
  RESULTS
  Gal-9 levels in the BALF were significantly higher in patients with CVD-IP than in patients with IIPs. Gal-9 levels significantly correlated with both the total cell count and the absolute number of lymphocytes in the BALF of patients with IIPs and CVD-IP. Strong reactivity with anti-Gal-9 antibody was observed in the cytoplasm of alveolar macrophages, lymphocytes, and type II pneumocytes in the lungs of patients with IP. Gal-9 expression in those cells was more remarkable in patients with CVD-IP than in patients with IPF and idiopathic NSIP. Gal-9 suppressed the growth of human lung fibroblast cells in a dose- dependent manner. Gal-9 induced apoptosis of human lung fibroblast cells in a dose-dependent manner.
  
  
  CONCLUSIONS
  Our findings suggest that the expression level of Gal-9 in the lung is increased in patients with CVD-IP and that Gal-9 may have a protective role against pulmonary fibrosis of these patients.
authors: Neurology, Respirology, Endocrinology, and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan. nobuhiro@med.miyazaki-u.ac.jp
authors: Nobuhiro
authors: N
authors: Matsumoto
authors: Shigeki
authors: S
authors: Katoh
authors: Shigehisa
authors: S
authors: Yanagi
authors: Yasuji
authors: Y
authors: Arimura
authors: Masatoshi
authors: M
authors: Tokojima
authors: Masaki
authors: M
authors: Ueno
authors: Mitsuomi
authors: M
authors: Hirashima
authors: Masamitsu
authors: M
authors: Nakazato
mesh_terms: D000368:Aged; D017209:Apoptosis; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D016022:Case-Control Studies; D049109:Cell Proliferation; D002478:Cells, Cultured; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D037161:Galectins / Q000097:blood / Q000378:metabolism*; D006801:Humans; D054988:Idiopathic Interstitial Pneumonias / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D054990:Idiopathic Pulmonary Fibrosis / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D008168:Lung / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011994:Recombinant Proteins / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D037161:Galectins; C105032:LGALS9 protein, human; D011994:Recombinant Proteins