The lymphocytic alveolitis in sarcoidosis is associated with increased amounts of soluble and cell‐bound adhesion molecules in bronchoalveolar lavage fluid and serum

Berlin M, Lundahl J, Skold CM, Grunewald J, Eklund A (Karolinska Hospital and Karolinska Institute, Stockholm, Sweden). The lymphocytic alveolitis in sarcoidosis is associated with increased amounts of soluble and cell-bound adhesion molecules in bronchoalveolar lavage fluid and serum. J Intern Med 1998; 244: 333–340. Objectives 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. Design 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 α4-β1 (VLA-4) and α5-β1 (VLA-5) integrins on alveolar T-lymphocytes were analysed. Setting The subjects attended the outpatient clinic at the Division of Respiratory Medicine, Karolinska Hospital, Stockholm, Sweden. Subjects 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 β1-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.