title: Elevated concentrations of liver-expressed chemokine/CC chemokine ligand 16 in bronchoalveolar lavage fluid from patients with eosinophilic pneumonia.
abstract: BACKGROUND
  Eosinophilic pneumonia is characterized by the prominent accumulation of eosinophils and lymphocytes in the lung parenchyma. Liver-expressed chemokine (LEC)/CC chemokine ligand 16 (CCL16) is a novel functional ligand for H4 which is expressed on eosinophils and also an affinity ligand for CCR1, CCR2, CCR5 and CCR8 which are expressed on T lymphocytes and monocytes. The purpose of this study is to clarify the role of LEC/CCL16 in eosinophilic pneumonia.
  
  
  METHODS
  The LEC/CCL16 level was measured using an enzyme-linked immunosorbent assay in the bronchoalveolar lavage fluid (BALF) of 33 patients with eosinophilic pneumonia, 26 patients with sarcoidosis and 10 healthy volunteers. The cell sources of LEC/CCL16 in BALF were evaluated by immunocytochemistry.
  
  
  RESULTS
  The LEC/CCL16 levels in BALF from patients with eosinophilic pneumonia were significantly higher than those from patients with sarcoidosis and healthy volunteers. The BALF LEC/CCL16 levels correlated with the numbers of BALF eosinophils and lymphocytes, respectively. The BALF LEC/CCL16 levels were significantly decreased after remission in eosinophilic pneumonia. In immunocytochemistry, the LEC/CCL16 expression was clearly observed in CD1a-positive dendritic cells as well as in CD68-positive macrophages harvested from patients with eosinophilic pneumonia, but not from the controls.
  
  
  CONCLUSIONS
  These results suggest that LEC/CCL16 produced by dendritic cells as well as by alveolar macrophages contributes to the accumulation of eosinophils and lymphocytes into the inflamed lungs of patients with eosinophilic pneumonia.
authors.affiliation: Department of Internal Medicine 3, Faculty of Medicine, Oita University, Oita, Japan. nureki@med.oita-u.ac.jp
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Nureki
authors.forename: Eishi
authors.initials: E
authors.lastname: Miyazaki
authors.forename: Yuko
authors.initials: Y
authors.lastname: Usagawa
authors.forename: Takuya
authors.initials: T
authors.lastname: Ueno
authors.forename: Masaru
authors.initials: M
authors.lastname: Ando
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Takenaka
authors.forename: Takeo
authors.initials: T
authors.lastname: Ito
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Ishii
authors.forename: Toshihide
authors.initials: T
authors.lastname: Kumamoto
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000096:biosynthesis; D018949:Antigens, CD1 / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D001992:Bronchoalveolar Lavage Fluid; D019742:Chemokines, CC / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D018450:Disease Progression; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D016676:Macrophages, Alveolar / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011657:Pulmonary Eosinophilia / Q000175:diagnosis / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D012507:Sarcoidosis / Q000175:diagnosis / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D018949:Antigens, CD1; D015214:Antigens, Differentiation, Myelomonocytic; D019742:Chemokines, CC; C481939:CCL16 protein, human; C419393:CD1a antigen; C067980:CD68 antigen, human; D000097382:CD68 Molecule