title: The lymphocytic alveolitis in sarcoidosis is associated with increased amounts of soluble and cell-bound adhesion molecules in bronchoalveolar lavage fluid and serum.
abstract: OBJECTIVE
  Pulmonary sarcoidosis is a chronic inflammatory disorder of unknown aetiology accompanied by a lymphocytic alveolitis. It is likely that a selective and temporal expression of adhesion molecules plays a crucial role in the recruitment of cells to the inflammatory site. We investigated the expression of adhesion molecules on alveolar T-lymphocytes and in bronchoalveolar lavage (BAL) fluid and serum to elucidate mechanisms behind the accumulation of cells in the lung in sarcoidosis.
  
  
  METHODS
  In a cross-sectional study in patients with active and inactive sarcoidosis and in healthy volunteers, we examined, in serum and in BAL fluid, the soluble adhesion molecules, VCAM-1, ICAM-1, and P-, E- and L-selectin. In addition, the expressions of alpha4-beta1 (VLA-4) and alpha5-beta1 (VLA-5) integrins on alveolar T-lymphocytes were analysed.
  
  
  METHODS
  The subjects attended the outpatient clinic at the Division of Respiratory Medicine, Karolinska Hospital, Stockholm, Sweden.
  
  
  METHODS
  Nineteen sarcoidosis patients, nine with clinically active disease, and 13 healthy volunteers were included in the study. The sarcoidosis diagnosis was based on a typical histological and/or clinical (symptoms, radiograph, lung function) picture.
  
  
  RESULTS
  In sarcoidosis patients, particularly in those with active disease, an increase of the expressions of beta1-integrins was accompanied by elevated concentrations in BAL fluid of soluble VCAM-1. In serum, the levels of E-selectin and ICAM-1 were significantly higher in patients with active disease than in those with inactive disease and controls.
  
  
  CONCLUSIONS
  The findings offer some mechanistic explanations as to how the cell-rich alveolitis in sarcoidosis occurs, and furthermore suggest additional markers, such as s-ICAM-1, for assessment of disease activity.
authors.affiliation: Department of Medicine, Karolinska Hospital, Stockholm, Sweden. berlin@lung.ks.se
authors.forename: M
authors.initials: M
authors.lastname: Berlin
authors.forename: J
authors.initials: J
authors.lastname: Lundahl
authors.forename: C M
authors.initials: CM
authors.lastname: Sköld
authors.forename: J
authors.initials: J
authors.lastname: Grunewald
authors.forename: A
authors.initials: A
authors.lastname: Eklund
mesh_terms: D000328:Adult; D001992:Bronchoalveolar Lavage Fluid; D015815:Cell Adhesion Molecules / Q000097:blood / Q000378:metabolism*; D003430:Cross-Sectional Studies; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation; D016023:Integrins / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011650:Pulmonary Alveoli / Q000473:pathology*; D017565:Sarcoidosis, Pulmonary / Q000097:blood / Q000150:complications* / Q000378:metabolism*; D019087:Selectins / Q000378:metabolism; D013601:T-Lymphocytes; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D016023:Integrins; D019087:Selectins; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1